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July 22, 2019, 03:24:58 am

Author Topic: How to approach topic 2: infectious disease  (Read 45 times)

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Bri MT

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How to approach topic 2: infectious disease
« on: June 17, 2019, 09:30:27 pm »
Over units 1-4 I found learning about the immune system to be the most complex and difficult part of biology, but by the end I also found it engaging & could use it for easy marks. 

Here are my tips to go from where I started (overwhelmed) to where I ended (confident):

Breakdown key terms into their components

There’s going to be a lot of vocab and jargon you’ll have to learn, and it’s easier to understand and remember that if you can turn words from seemingly random jumbles of letters to units with meaning. Eg. “cytotoxic T cell”: ‘cyto’-> cell, toxic -> deadly & cytotoxic T cells kill other cells. Even the ‘T’ gives you information – T cell is another term for “thymus-maturing lymphocyte”. And you can break apart ‘lymphocyte’ into lymph & cyte….

You can also use this on phrases like "antigen presenting cell" it's a cell. That presents antigens.  (I'm glad biologists haven't ben very creative in the past :P)

Revise the terminology

If you follow the suggestion above you'll hopefully find it easier to remember the terminology but chances are you'll still need to revise it. You don't want to be learning about antibodies agglutinating pathogens only to realise you have no idea what those 3 words mean. It can be easy to be confused by the terminology so creating and practicing a flashcard glossary is a good way of making sure you can figure out what's going on and don't get lost.

Make and use diagrams
Diagrams are fantastic for showing lots of content in a clear and understandable way. This includes flowcharts showing processes such as the humoral response, labelled diagrams for plant defence strategies, mind maps for disease control strategies, and ven diagrams contrasting similar topics.   


There are many practice questions available on immunity which will allow you to check your understanding and practice application. It’s important to remember the terms, but straight recall alone won’t be enough to maximise your marks – and until tested it’s hard to know how good your memory truly is. It can be demoralising to get questions wrong, but each time you correct an incorrect answer you’re a step closer to getting it right.

Below there are many questions on immunity which you can use to test yourself and learn a bit more. If you still have any questions please feel free to
 register here for FREE to ask any questions you may come across in your QCE studies! and head over to the biology Q&A.

As always, feel free to reply to this with any questions about this or what's worked (or not) for you :)

U3 AOS 2 Responding to antigens part 1

Do some antibodies remain in the body after an immune response?
I just want to clarify that after an immune response, there will still be some antibodies circulating the system despite most of it being broken down? Or are all antibodies produced by plasma cells at the time of infection broken down and just the memory cells remain?
Yeah, some antibodies specific to the antigen will remain in circulation after the infection is gone (with the concentration gradually reducing over time)
What is the difference between cytotoxic T cells and natural killer cells?
What is the difference between cytotoxic T-cell and natural killer cells?
Cytotoxic T-cells are part of the cell mediated specific immune response, whereas natural killer cells are part of the non-specific immune response; T-cells recognise antigens, whereas NK cells do not.
This is outside of the scope of the VCE course, but its some extra interesting info about it and you can find it in the Nature of Biology textbook if you use it. So basically, Natural Killer cells have two receptors, a killer activation receptor (KAR) and killer inhibitory receptor (KIR). KAR binds with surface proteins released by virally infected cells or cancerous cells in distress, while KIR binds to MHC Class I markers on the cell. If the KIR binds with a sufficient number of MHC Class I markers, then the order to kill is overridden. (We can get a lack of MHC Class I markers when viruses or cancer cells inhibit or destroy MHC Class I markers on the cell surface). Therefore, if the cell is lacking of MHC Class I markers, then the signal to kill won't be overridden and then the NK cell will secrete perforin damaging the plasma membrane leading to lysis. If the cell has sufficient MHC Class I markers, then I'm pretty sure that those cells are left for cytotoxic T cells.
What is the difference between lymphocytes and leukocytes?
Also what is the difference between lymphocytes and leucocytes?
I think leukocytes are the general term for cells of the immune system, whereas lymphocytes are those that are part of the specific immune system such as T and B lymphocytes.
Just to add to this, NK cells are also lymphocytes even though they're not a part of the adaptive immune response (they're innate and non-specific). Leukocyte is the scientific name for white blood cells.  :)
What is the role of cytokines in the immune response?
What is the role of cytokines in the immune response?
Cytokines: Proteins produced by all cells of immune system which act as intracellular messengers to convey signals within the immune system. Interleukin is a key example of a cytokine. IL-1 resets the hypothalamus (creates fever) and recruits T- Helper cells) while IL-2 activates B cells (which is the humoral response) and activates T-Cells (which is a cell-mediated response)
What are the functions of the five types of immunoglobins (antibodies)?
Does anyone have a list of definitions and functions for the 5 type of immunoglobulins?

Thanks :)
-IgG - Has a life span of 21 days, mostly circulating antibodies and function in agglutination and complement activation.
-IgA - Has a life span of 6 days, found in external secretions, tears, saliva and milk. Functions as mucosal immunity.
-IgM - Has a life span of 10 days, produced early in infection response and function in agglutination and complement activation.
-IgE - Has a life span of 2 days, produced in allergic reactions and attaches to mast cells.
-IgD - Has a life span of 3 days, located on the surfaces of antibody-producing cells (B lymphocytes)  and are responsible for the development of antibody response.

The SD doesn't explicitly say to know these. However IgD and IgE are two I would make sure I knew. :)
Do all pathogens cause disease?
Do all pathogens cause disease? If not why? I was under the impression that an infectious disease is caused by a pathogen, but my text book tells me not all pathogens cause disease.
Firstly, a pathogen is a "disease-causing organism or agent". However, this does not necessarily mean that every pathogen brings about disease in a host; rather, they may have the potential to cause disease (pathogenicity), but the host's immune responses prevents it from doing so. Or sometimes, they only cause disease under certain conditions/circumstances (e.g. opportunistic pathogens).

This is because a disease is defined as that which harms the normal functioning of the body. So if an organism is not 'harming' the body, then it's not acting as a "disease-causing agent".

Edit: yes, an infectious disease is always caused by a pathogen, by not all pathogens get the chance to cause disease in a host organism.
What is the role of antibodies?
What is the role of antibodies? Do they bind with antigens to help facilitate phagocytosis by clumping them together or is there more to it?
More to it, but that's one thing they do. They can neutralise things that come in and they can also promote phagocytosis as you suggested. They're also pro-infammatory and can activate complement.
What is the purpose of MHC markers?
What is a perfect definition of an antigen?
What is a perfect definition of an antigen which would get full marks?
5. A foreign body that induces the production of antibodies. (antibody generating).
How do helper T cells activate B cells?
Anyone know how a helper T cell activates the other lymphocytes?  :-\
Most B cells require 2 signals to be activated and begin clonal proliferation and differentiation into plasma and memory cells:
1. B-cell receptor binds to specific antigen.
2. T helper cells (which have been activated by that specific antigen) then secrete cytokines/interleukins (messengers between immune system cells) which bind to and stimulate/activate the B cell.

So essentially, B cells can't multiply and become antibody-producing plasma cells just by running into the appropriate antigen; they NEED a T helper cell to send them cytokines.  You don't have to know more than this (e.g. what the specific cytokines are, or how it all works).
How do cells detect non-self material?
Hey guys,

 I was just wondering if someone could give me a summary of how cells detect foreign materials from self materials, which cells detect this and how cells detect viruses? Another thing I am not fully understanding is the MHC markers.


There are a number of ways that cells can recognise non-self. Certain cells of the immune system express receptors that can bind molecular markers that are relatively common in pathogens but never appear in humans. For instance, these receptors might bind double-stranded RNA, which occurs in some viruses but certainly not in human cells.

B-cells express receptors that are able to bind free antigens. These are molecules that are part of or produced by pathogens that float around in tissue. B-cells can bind a whole host of these molecules. They do not, however, typically express receptors to self molecules (how this happens is well beyond the course but basically any B-cells that express receptors to self antigens are deleted).

T-cells, on the other hand, express receptors that can bind antigens (i.e. molecules from pathogens) that are presented on MHC markers. MHC class I markers present antigens (they just hold them) that originate from inside the cell. Therefore, if a cell is infected by a virus, molecules from the virus are expressed on the surface of the cell. T-cells will recognise these molecules as foreign and will respond accordingly. MHC class II molecules are expressed on a limited number of cells. These molecules present antigens that have come from the environment. T-cells can bind antigens presented on these MHC molecules if they are non-self.

What’s the difference between antibodies, antigens, and MHC markers?
Hey everyone

I keep getting confused with antibodies, antigens and MHC markers. Can someone please distinguish them for me? I have not done immune system before so any help would be greatly appreciated. <3

Antigens: they are group of compounds, typically proteins which provoke/trigger an immune response, including the production of antibodies.
Antibodies: protein molecules designed to attach to only one specific type of antigen.
MHC Markers: In order to to distinguish non-self from self molecules, MHC markers are located on the surface of cell membranes.
Class 1 MHC Markers: located on the surface of all human cells with a nucleus (except RBCs). They display peptide fragments produced within the cell.
Class 2 MHC Markers: located on antigen-presenting WBCs. They present peptide fragments that they have engulfed via phagocytosis.

Physical and chemical plant defences?
what plant defences (both physical and chemical) are we required to know for the exam? If a question asked to list a few physical and chemical plant defences, what could you say?
*pulls out VCAA definitions and processes document*

(surprisingly, it's really handy for myself too :D) So these are answers from past questions they've asked:

Barriers in plants:
•   Waxy layers on outside surface
•   Intact or thick cuticle
•   Chemicals that repel potential pathogen vectors such as insects
(Not from the exam report but my own knowledge: another could be thorns and hairs to deter vectors, or excreting nasty chemicals that kill pathogens - no need to be specific)

And if infection does occur in plants:
•   Grow ‘gall’ tissue round area containing infective agent to prevent spread to other areas
•   Produce chemicals e.g. tannins
•   Produce ‘gum’ to seal off wounded area
•   Drop infected leaf to inhibit spread to other areas
What happens to a macrophage after it engulfs a foreign pathogen?
When a macrophage engulfs a foreign pathogen, it digests and degrades it. Antigenic fragments are then presented on the MHC II markers. What happens now? Where does this macrophage go, or what comes to it?
The activated macrophage will carry the antigen (on its MHC class II) to the lymph nodes, where T cells are accumulated, improving the chance of finding the matching helper T cell.
The macrophage then releases interleukin-1 to activate helper T cell.
Can the 2 variable regions on an antibody be different?
Can the two variable regions on an antibody be different?
Thanks  :)
the variable region has to be identical because it is specific for a particular antigen.
Why do phagocytes have a large number of ribosomes?
Why do phagocytes have a large number of ribosomes?
Help would be greatly appreciated.
Thanks in advance
Phagocytes need lots of ribosomes to manufacture digestive enzymes which fill the lysosomes to destroy any foreign material engulfed by the cell.
How are B cells activated?
Hey  :)

Could someone please explain to me how B Cells are activated? And the role of T Helper Cells in activating the B Cells, I'm confused  :'(
B-cells get activated when they bind to a specific antigen. It will then proliferate and differentiate into two different cells 1. Memory cells, basically the same as the parent cells(same antibody for the specific antigen) and plasma cells, these produce and secrete anti-bodies for the specific antigen.
T helper cells can only bind to antigens located on the MHC 2 protein in contrast to cytotoxic T cells. T helper cells activate B-cells by releasing cytokines to the B-cell that it is binded to. *Im sure these are correct, but if there is anything wrong, feel free to correct me*
Can APC’s only present antigens to Tc cells?
2) Can APC's present antigens to cytotoxic t cells as well or just helper t cells?
2.APCs can present to both. Antigens on MHC2 markers will be presented to T helper cells and antigens on MHC 1 markers will be presented to cytotoxic T cells.
Just to clarify: They can only present antigens whilst performing their function to a Th cell. However, they can also present fragments of their own polypeptides to Tc cells, as all cells can do (except red blood cells).
How can we identify a pathogen?
Also, how do we identify pathogens?
There are actually a few ways to identify a pathogen (bacteria or virus, in this case)
- agglutination test (with specific antibodies)
- precipitation test (to see if a bacterial colony precipitates in the blood of an infected person)
- Western blot test (used to separate and identify proteins specific to a bacteria)
- ELISA (enzyme-linked immunosorbent assay, which is used to detect and count substances such as antibodies, hormones, enzymes and antigens, which indicates the type of bacteria we might be looking for)
Virus (these things are smaller, so we have to use more precise techniques to kinda sort them out)
- X-ray crystallography (which is used to determine the atomic and molecular structure of crystals, can be used to identify viruses of specific shapes and sizes)
- Electron microscope (these things let you see really small things so you can see viruses with this)
How are cytotoxic T cells activated?
Hi all,
Can somebody please explain how Tc cells are activated? Do they require Helper T cells at all?
Thanks in advance :)
My understanding is that Helper T cells bind to infected cells and release cytokines which attract Tc cells. Then the Tc cells bind to the virus-infected cell and secrete perforins, inducing lysis.
Hi!  :D

Cytotoxic T cells recognise and bind to the antigens presented on the MHC-I markers on cells that are cancerous or virally infected and the binding of the Tc receptors causes a signal transduction in the T cell, resulting in it proliferating and differentiating into active Tc cells and memory T cells. And I'm pretty sure that the cytokines that the helper T cell produces helps the Tc cell to proliferate and differentiate.

The Tc cell then releases perforin to destroy the plasma membrane of the infected cell to kill it or may kill it by binding to the infected cell's death receptor.

*someone please correct me if neccessary  :)
Both answers above are pretty close.

Cytotoxic T-cells do bind to MHC class I molecules on cells that are infected with an intracellular infection. Cytokines from multiple sources help to stimulate the T-cells, as do signals directly from T-helper cells.
How are B and T cells activated?
Can someone please tell me how B and T cells are activated, the answers my teacher and the exams give are so ambiguous  :'(
B cells are activated by free antigens (ie parts that have broken off) binding to them. T helper cells are activated by an antigen that they can bind to being presented to them on MHC 2 markers by an Antigen Presenting Cell (APC) ie. dendritic cells and macrophages.The activated B cells and T helper cells then find each other and if they have the same specificity (have bound the same antigen) the T helper cell will release cytokines (a type of signalling molecule) that further stimulate both of them to divide and differentiate. Cytotoxic T cells are activated when they can bind to a peptide fragment presented on an mhc 1 molecule. They can also be further stimulated by the cytokines but do not need to interact with t helper cells.
What causes histamine to be released?
1. What are the causes of the release of histamine?
1. There are many causes: Damage to the surrounding tissue, cross linking of bound antibodies (an allergic response), it can also be released by some medicine (including morphine and some antibiotics - but we don't need to know this)
Overview of intracellular (cell-mediated) immunity
General process always occurring in our bodies:
-B cells mature in the bone marrow. Here they are tested for self-reactivity, if they can bind to a self antigen they are normally destroyed (except for malfunctions ie autoimmune diseases.)
-Both Tc cells and Th cells mature in the thymus gland. Here they are also tested for self reactivity.

Throughout the body there are always B cells, Th cells, and Tc cells with a randomly generated antigen specificity.
B cells are found in lymph nodes (and throughout the lymph system)
Th cells are found in lymph nodes
Tc cells are found throughout the body tissues.

B cells and Th cells just hang about waiting for their antigen to bind/be presented to them.
Tc cells travel throughout the body attempting to bind to peptide fragments presented on MHC1 markers.

If an intracellular pathogen (ie virus) enters the body, parts of it will inevitably end up in the blood and lymph. Some of it will enter cells and cause the creation of non-self peptide fragments which will be presented on MHC 1 markers at some point. The following will happen simultaneously.

Humoral Immunity will be activated:
-A naive B cell will bind to a free antigen (ie. not presented by an APC).
-A Th cell will be presented with its antigen on a MHC2 molecule by an APC.
-The 'selected' B cell and Th cell will then find each other and if they have bound the same antigen, the Th cell will release cytokines (the same cytokines that affect cell mediated immunity - see below.)
-These cytokines cause the B cell to divide (proliferate) and differentiate into B memory cells and B plasma cells.
-These cytokines also cause the Th cell to divide (proliferate) and differentiate into Th memory cells and Th active cells.
-The memory cells remain in the body to fight subsequent infection by a pathogen with the same antigen specificity and the B plasma and Th active cells fight off the current infection.

As the pathogen (virus) is intracellular, cell mediated immunity is also activated.
-Naive Tc cells are always travelling throughout the body, attempting to bind to peptide fragments presented on MHC1 markers.
-When they find one that they can bind to, the Tc cell is 'selected'.
-The Tc cell will release granzymes (including perforin) which causes the cell to undergo apoptosis.
-The Tc cell continues to travel throughout the body and kill cells presenting the same peptide but it will not divide and differentiate until cytokines are present.
-When cytokines have been released from Th cells (this could happen before or after the Tc cell is selected) the Tc cell will divide (proliferate) and differentiate into Tc memory cells and Tc active cells.
-The Tc memory cells will remain in the body to fight off subsequent infection by the same pathogen.
-The active Tc cells will travel throughout the body, inducing apoptosis in cells presenting the same peptide fragment.
What is the role of cytokines in the immune response?
What is the role of cytokines in the immune response?
Cytokines: Proteins produced by all cells of immune system which act as intercellular messengers to convey signals within the immune system. Interleukin is a key example of a cytokine. IL-1 resets the hypothalamus (creates fever) and recruits T- Helper cells) while IL-2 activates B cells (which is the humoral response) and activates T-Cells (which is a cell-mediated response)
What are antigens?
Are antigens always referred to as foreign substances; don't all cells have antigens even self cells?
No, antigen means anything that generates an adaptive immune response.
Antigens are not always foreign but the ones your body actually mounts a full fledged immune response to are usually foreign.
antibody generating
Does tissue rejection involve natural killer or cytotoxic T cells?
When tissue rejection occurs, do only NK cells attack the 'non-self' tissue? Can it also be Cytotoxic T cells? Thanks.
CTL can definitely attack non-self tissues.  NK cells can't technically differentiate between self and non-self in a specific sense because they are innate cells.  CTL are the ones that will recognise specific non-self proteins on the surface of the cells.
Are needles vectors?
Also can vectors include needles?
Needles can't be vectors - vectors need to be living things that can carry an infectious organism from one host to another.  A needle is closer to a fomite.
What is Clonal Expansion?
Could someone explain the basics of Clonal Expansion? Everywhere I look is confusing and too complex haha
clonal expansion just refers to the differentiation of B cells which are part of the humoral response. B cells can produce 2 cells including B-plasma cells and B-memory cells.
Would you say T helper cells initiate clonal expansion?
Yes. They would have to initiate clonal expansion of certain B-cells/T-cells (that have a specific antibody-like receptor to the antigen)
Do antibodies in the body remain higher after a secondary immune response?
In the secondary antibody response why does the level of antibodies in the bodily fluids remain higher for a longer period of time than in the primary antibody response?
Well in Humoral immunity, T helper cells initiate the differentiation of B cells when exposed to a non self cell. The B cells become either memory or plasma cells, the memory cells remain in the body for a longer period of time, providing a rapid immune response (the secondary response). This is achieved by developing plasma cells much quicker than previously, destroying the pathogen before it can affect the host. Also known as the immunological memory.
What is the difference between MHC markers and antigens?
What is the difference between MHC markers and antigens?
MHC markers are proteins that are on a cell which indicates to the organism's immune system that it is a self cell. Examples of cells with MHC markers include macrophages, B cells and dendritic cells. An antigen are also proteins, an agent; pathogen, that 'binds' to an antibody, initiating a immune response.

However MHC markers, in the instance of an organ transplant can go under 'attack' as they are recognised as non-self cells as that organ does not possess the appropriate MHC markers.
What causes swelling and itchiness in the inflammatory response?
Does the swelling from inflammation result from leaky capillaries or vasodilation which brings more blood to the site?

Also, what causes the itchiness from inflammation?
Leaky capillaries causes an accumulation of fluid in the tissues, causing the swelling. This fluid carries phagocytes to the sites of infection.

Itchiness/pain is probably a result of increased pressure on surrounding nerves due to that swelling.
What is the difference between a leucocyte and a lymphocyte?
What's the difference between a leucocyte and a lymphocyte?
Leukocyte is a white blood cell
Lymphocyte is a group of white blood cells (T-cells and B-cells)
Function of MHC1/MHC2?
Hey guys, can somebody please help me out with MHC markers, I'm still quite confused about them! From what I understand:
MHC Class 1: Found on all nucleated cells
MHC Class 2: Found on B and T cells and macrophages
Could someone please help me with the function of each class and anything else we should know about them? thanks :)
MHC class I presents things that are inside the cell, whereas class II presents things that have been found in the environment. So if there's a virus in a cell, that'll pop up on class I and will "encourage" the immune system to kill it.
MHC 2 - Found on APC that present antigens to Helper T cells, which relay messages to either B or T cells with cytokines to begin proliferation
Please explain the differences between MHC1 and MHC2
can somebody please explain the process of macrophages and displaying MHC1 markers?
-Macrophage encounters a non-self antigen expressed on a pathogen/agent/substance, engulfing it. 
-The engulfed substance travels in a vesicle within the macrophage and fuses with a lysosome, where it is broken down into fragments.
-One of these peptide fragments then complexes with an MHC II and is expressed on the plasma membrane of the macrophage.
-Macrophages are APCs, therefore they possess MHC II molecules for the sole purpose of signalling the adaptive immune response upon foreign invasion.

Every nucleated cell (therefore not RBCs) expresses MHC I. Consequently, MHC I are 'self' detectors. As all MHC receptors have the capacity to express peptide fragments, infected cells will have foreign proteins complexed with their MHC I receptors. Normal cells will possess 'self' peptides complexed with their MHC I molecules. This establishes the differentiation between 'self' and 'non-self'

Therefore, MHC I does express 'self', HOWEVER upon infection (say by a virus) the molecules will express obscure peptide fragments which indicates to the immune system that the cell is not healthy. Then, NK cells (antigen non-specific) or Tc cells (antigen specific) will destroy the affected cells.

I hope that makes sense :)
Difference between primary and intermediate (secondary) host?
Can someone please distinguish between a primary host and an intermediate host? Cheers!
Primary host --> Host that the adult parasite lives in/on

Intermediate host --> Host that the larval parasite lives in/on
Primary host: site of sexual reproduction
Secondary host: site of asexual reproduction
Do plants have specific immunity?
Do plants have specific immunity? If yes, can someone please explain the concept? Thanks!
No. Plants only have physical and chemical barriers to stop pathogenic agents from entering the internal environment of the plant organism. This includes things like the formation of galls to trap and prevent the spread of a pathogen, etc. No specific attacks are made against specific strains of pathogens, and no memory is involved.
Does that mean plants die if a pathogen gets into their internal environment?
Thanks Yacoubb! So if a pathogen does manage to enter into the internal environment, does the plant have no other choice but to essentially die? Do plants possess anything similar to the mechanisms of a white blood cell?
There are different means by which the plant can try to protect itself. For instance, the formation of a gall. This gall is just a mass of tissue that forms around the site where the pathogen enters, which traps the pathogen, and prevents it from spreading to other parts of the plant.

However, its more than likely the plant will die if it is infected by a pathogen, because of its limited immunity to pathogenic agents.
What are the differences between basophils and mast cells?
What are the differences between basophils and mast cells, are they interchangeably used in inflammation, allergies
Relatively carry out similar functions; however differ in origins, sizes, shapes of nucleus, and their locations in the body. Are responsible for similar allergic reactions, and they both are made in the bone marrow, however, they are derived from different progenitors. As basophils mature in the bone marrow then travel throughout the blood stream, whereas mast cells leave the bone marrow in an immature state, and mature in body tissues.

In the case of inflammation, my thought is that they are interchangeable as both produce histamines. Not too sure about that one though!
(might want to check up on that)
If you're discussing inflammatory or allergic reactions, refer to mast cells, not basophils. Basophils are very unlikely to come up in the exam
How do mast cells help kill pathogens?
Is someone able to help me out with the inflammatory response?

I understand that mast cells release histamine which causes blood vessels to dilate, drawing more blood to the region and increasing heat, redness and swelling.

What I don't understand is how this actually kills the pathogen?

It facilitates the process
Exactly what grannysmith said, it literally makes the blood vessels more permeable and hence the phagocytic cells are easily transported to the damaged tissue.
Local dilation of capillaries --> blood flow through area is more rapid (which may cause erythema) --> phagocytes can be transported to area more rapidly and destroy

Release of histamine increases permeability of local capillaries --> phagocytes more rapidly able to diffuse out into the interstitial spaces. Plasma also leaks excessively from the capillaries and accumulates in the interstitial spaces (plasma leaks more rapidly from capillaries than it can be returned to circulation via the lymph vessels), which causes swelling
Simple explanation of humoral and cell-mediated immune response
Can anyone give me a simple explanation of humoral and cell-mediated response?
Simple? I don't think thats possible haha!

Well Humoral and Cell-Mediated responses fall under the 3rd line of defence also known as the specific/adaptive immunity.

  • B-lymphocytes are the major cells involved.
- Produced in the Bone Marrow (thus the name B-lymphocytes)
  • Each B-Cell has its individual antibody/antigen complex
  • Production of antibodies
  • B-Cells differentiate (clonal expansion) into
- B-Plasma cells (effector cells): secrete antibodies
- B-memory cells: remain in the body so when the antigen is encountered again, a response can rapidly be reenacted.

  • Carried out by T-Cells
  • T-Cells made in the Bone Marrow however matured in the Thymus (hence its name  T-Cells)
  • T-Cells include; Helper T cells (Th), Cytotoxic T cells (Tc) and Suppressor T cells.
  • Helper T cells active cytotoxic cells and present antigens to immature B cells.
  • Cytotoxic cells detect/recognise cells with infection, are able to destroy these foreign cells with contact
  • Lastly Suppressor T cells, literally suppress the immune responses once the antigen has been removed
How do antibodies work?
Do antibodies, when they attach to antigens, inactivate the antigen themselves? Or do they act as a marker to attract other cells to engulf the antigen?
Antibodies; are proteins that bind and neutralise antigens. Are quite specific (like an enzyme-substrate complex).
Antibodies do not engulf the antigen. They bind to it and make it easier for phagocytes to find. They also make the antigen larger. This can stop them from working (e.g. They cause snake venom to agglutinate).
Do all Antigen presenting cells have MHC2?
Do all antigen-presenting cells have MHC class-2 markers?
Yes. Antigen-presenting cells such as macrophages, certain B cells and dendritic cells express MHC class II. The fragment of the antigen is bound there for the T cell to recognise.
What are granulated cells?
What are granulated cells and how does granulation assist in their functioning?
Granules are small packets of enzymes and other substance for example inflammatory chemicals like histamine. --> that are made up by Leucocytes that assist them in performing their function. For those white blood cells that are phagocytic (macrophages, etc) the enzymes in the granules (vesicles) will be released onto the eaten foreign material and break down its component pieces; hence bacteria is killed. The enzymes have to be kept in these designated vesicles because if they were free inside the white blood cell, they would destroy it from the inside.

Hope this helps :)
What is the cell mediated response? What do MHC markers do?
Can somebody please explain the cell mediated response?
also, where do MHC markers come into play
The cell mediated response is basically when the cytotoxic T-cells directly acts upon the virus/cancerous/fungi affected cells. For example, when a phagocyte (or other antigen presenting cells such as dendritic cells) engulf the pathogen (which could be a virus) it presents the non-self antigen fragments of the pathogen on its MHC marker on the surface of the cell membrane. The MHC marker in this case basically acts like a 'stage', kind of like a 'trophy holder' and stimulates the T-helper cell. The type of the marker would be class-2 since it is an antigen presenting cell and the stimulation of the T-helper cell would occur by interleukin-1 or you can just say cytokines and also matching receptors. The T-helper cell will then stimulate inactive T-lymphocytes to undergo clonal expansion and to differentiate into cytotoxic-T cells, T-supressor cells and T-memory cells.
The cytotoxic-T cells destroy virus-infected cells by releasing perforins (a kind of protein) which punches holes and lyses the membrane of the infected cell.

I hope this helps you somewhat and please, anyone correct me if I am incorrect!

(EDIT: beaten :P)
What’s the difference between mast cells and basophils?
Are Mast Cells and Basophils the same thing? Other than promoting an inflammatory response and blood flow through the secretion of histamines, do they have different distinct functions?

Quite confused tbh :/ Our teacher hinted to say Mast Cells instead... however is there a difference? Or is it just a different name?
They are different cells.  Basophils usually move through the circulation whereas mast cells are localised to the tissues.  They have similar functions and coordinate similar responses :)
Mast cells usually act earlier in the response (eg allergic response) because they're localised to the tissue.  They can recruit basophils to the site from the circulation.
What’s the difference between a parthenogenic organism and a parthenogenic agent?
What's the difference between a pathogenic organism and a pathogenic agent ??? Thanks ! :)
Organisms are living, agents are usually reserved for viruses, viroids, prions which are non-living
Why does first exposure to an allergen produce less severe symptoms?
Explain why first exposure to an allergen produces less severe symptoms than subsequent exposure
I know it has something to do with memory cells.
2 main reasons are: B-memory cells have already been produced after fist encounter => response faster, more cross-linkages occur between the allergens and IgE antibodies bonded on mast cell, the release of histamine will also increase on second exposure.
What is the difference between a macrophage and a phagocyte?
What is the difference between a macrophage and a phagocyte?
A macrophage is a type of phagocyte. There are other types of phagocytes such as neutrophils and dendritic cells.
Similarities and difference between Natural Killer cells and cytotoxic T cells
Are natural killer cells and cytotoxic T-lymphocytes similar in function? I understand that natural killer cells are non-specific and are therefore a part of the 2nd line of defence, however both kinds of leukocytes destroy infected cells, right? They both secrete perforin and destroy cells which display MHC-1-antigen complexes, right? Can someone please clarify the similarities and differences between both cells :)
Yup, they have similar function.  The major difference is NK cells are innate (as you have said) so they don't recognise specific antigens.  NK cells kill without a TCR and without needing to recognise a nonself antigen whereas T cells must recognise a nonself antigen expressed on MHC in order to kill, and T cells have a TCR.
Both the similarities you have listed hold true.
What is MHC?
what is the major histocompatability complex and class 1 + 2 markers?
This excerpt from my notes might help :) -

MHC class I- found on all cells with a nucleus (therefore not red blood cells)
MHC class II- found on professional APCs (antigen presenting cells) like macrophages, dendritic cells and B- and T-lymphocytes.

The major histocompatibility complex itself is a complex of genes that code for MHC (major histocompatibility complex) markers. These markers are unique in every human (excluding identical twins), and are protein molecules which are ultimately located on the surface of cell membranes. They are examples of self molecules.

Foreign antigens as well as self antigens can be displayed on the MHC markers. These can, however, only be peptide antigens. MHC markers can therefore aid in distinguishing between self and non-self.

Cytotoxic T-lymphocytes register MHC I markers
Helper T-lymphocytes register MHC II markers

T-lymphocytes are MHC restricted, whereas B-lymphocytes are not.
What’s the difference between cell-mediated and humoral immunity?
The difference between cell-mediated and humoral immune response..

Would this response be acceptable?
-Cell mediated immune response involves the action of the T Cells whereby T helper cells bind to the antigen fragment on macrophages and activate cytotoxic T cells whereas humoral response involves the production of antibodies against antigens by B Cells
It's too verbose.

The cell mediated response involves T-cells whereas the humoral response primarily involves antibodies, which are produced by B-cells.
Are antibodies produced by B cells or plasma cells?
are antibodies produced by the b cell or the plasma cell? Which one is more correct? My teacher says only plasma cells
When B cells are activated, they differentiate into plasma cells and B-memory cells. Plasma cells produce free-floating anitbodies and release into the bloodstream, they have a pretty short life span.
Are mast cells involved in the inflammatory response?
are mast cells involved in the inflammatory response as well as, the allergic response?

Yes. They are the granulated cells that produce histamines.
Why does subsequent exposure to the same antigen result in a faster and larger immune response?
Why do subsequent exposures to a pathogen generate a greater and faster production of antibodies specific to the antigen? I know that this is primarily due to memory cells, but how/why exactly do they produce a greater and faster amount of antibodies? Wouldn't they have to go through the same process of clonal selection and expansion?
Remember that when a pathogen invade the body for the first time, there is hardly any antibodies in the blood that can combat with that pathogen. It takes the whole process of macrophage engulfing, advertising antigen on its MHCII blah blah blah until that antigen is identified by a B cell and antibodies are produced and that's why symptoms start to occur because it takes a long time. That's the primary response. However, in the secondary immune response, since now you have a larger concentration of antibodies for that specific pathogen inside your body (the antibodies that produced from plasma cells in the previous infection and a large amount of B-memory cells), this process gonna be much quicker, since now your cells have the memory and greater number of cells that can attack that pathogen much more quickly. This is the reason why, after successive immune response to the same pathogen, you might not even realise the symptoms because the large amount of antibodies from the previous infection has already destroyed it.
Just like for the first time, you have 1 machine running to do 1 job, now, you have 100000 machines running just to do the same job.
Can cytotoxic T cells kill cancerous cells? How?
Also, can cytotoxic T cells kill cancerous cells? Cancerous cells would exhibit an abnormal/altered MHC I marker without presenting an antigen fragment, and hence Natural Killer cells would be able to destroy them. However, considering killer T cells activate when they bind to an antigen-MHC I complex of another cell, would this mean cancerous cells are out of the picture?

Edit: I'm pretty sure they can kill cancerous cells, so the question is - how?
Yup, cancer antigens are also considered non-self because they wouldn't have been present in the thymus during T cell development.  Therefore T cells specific for cancer antigens also exist in the naive T cell population and can become activated and form CTL that can kill cancerous cells.  NK cells can also kill them if they have downregulated MHCI, as you have said. So you have two lines of defence against cancer - innate and adaptive :)
The cancer cell expresses the same MHC molecules as what would be present on any other cell but potentially at a reduced frequency.  However, because cancer is caused by a mutation in the genetic material of the cell it might produce abhorrent proteins (antigens) that wouldn't be found in normal cells on those MHC molecules - these proteins are recognised as non-self by the immune system in the context of the same MHC that would be present on noncancerous cells.  It's as if the cell were infected with a virus - presenting the foreign antigen on its surface in the context of MHC, but instead of their being an exogenous agent the cell has just mutated a protein so it is no longer considered 'self'.  Does this make sense?
Why do antibody levels remain higher for a long time after a secondary immune response?
In the secondary antibody response, why does the antibody level remain high for a long period of time after the infection has cleared, in contrast with the primary antibody response in which the antibody level decreases after the infection has cleared?
This is simply a result of having more B memory cells, meaning that it takes longer for them all to deplete.

I mean, it might also be a product of the body's capacity to recognise that subsequent infections reflect the antigen is present in the environment as a consistent threat... But I don't know if that's the case.

You would very rarely be asked to justify this in an exam though. Just know the graph that indicates heightened response and longer term immunity.
Why are antibiotics ineffective against viruses?
Why are antibiotics ineffective against viruses?
Antibiotics generally damage cell membranes, interfere with metabolism or affect cell walls, all of which are not found in viruses.
Can phagocytes detect non-self antigens?
Can phagocytes detect non-self antigens on the surface of pathogens and foreign substances?

Is this what causes them to engulf foreign pathogens in the innate immune response?
Yep, things like macrophages and neutrophils.
What are examples of barriers against food and water borne pathogens?
Barriers against food and water borne pathogens would include stomach pH and digestive enzymes, right? Because they're ingested the pathogens have already 'entered' the body, so the usual defences such as intact skin would surely not be applicable?
Correct. Stomach pH and digestive enzymes are still considered to be in the first line of defence as they are 'external' chemical barriers.
They are external as the gastrointestinal tract is open at both ends.
Questions originally from here
VCE: Sciences, eng lang & methods
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