VCE Biology Question Thread

[cosine]

So once a dendritic cell activates a specific T-helper cell by the use of interleukin-1 a T-helper cell becomes activated,  are memory T-helper cells produced and does the single T-helper cell undergo clonal expansion?

Correct, but the clonal expansion is not required for vce (only for B cells)

[adnauseam]

is it RNA polymerase that unwinds double stranded DNA into separate strands during transcription.
And would saying RNA polymerase joins RNA nucleotides that have annealed to template strand via complementary base pairing be alright?

[Elizawei]

(CSE 2014 test)
The answer for this question is B.
But I thought only nucleated cells, not bacteria,  have MHC class 1 markers? Or am i mistaken. 

[Sine]

Just to clarify

common sense suggests that memory T-helper cells are produced, however I've never come across a single question which referred to this or even stated this as a MC answers.

Are Memory T-helper cells produced the humoral/cell mediated responses?

[vox nihili]

is it RNA polymerase that unwinds double stranded DNA into separate strands during transcription.
And would saying RNA polymerase joins RNA nucleotides that have annealed to template strand via complementary base pairing be alright?

No, DNA helicase does.
YOu'd probably get away with it, but it's not technically correct.

Just to clarify

common sense suggests that memory T-helper cells are produced, however I've never come across a single question which referred to this or even stated this as a MC answers.

Are Memory T-helper cells produced the humoral/cell mediated responses?

Cell-mediated

(CSE 2014 test)
The answer for this question is B.
But I thought only nucleated cells, not bacteria,  have MHC class 1 markers? Or am i mistaken. 

(Image removed from quote.)

The answer is glycopeptidase chains. It's an unfair question, I'd just ignore it

[sunshine98]

In VCAA 2011 U3 question 1b ,
The question pointed to chloroplast and asked the type of nucleic acid present and to explain its function-
- I wrote: cpDNA - which encodes for enzymes needed during photosynthesis
-VCAA said: (chloroplast) DNA - which controls production of proteins for photosynthesis
Do I get the two marks (one for the correct name , and one for correct explanation) ?

anyone?

[Biology24123]

anyone?

You would get 2 marks if the question was worth 2 marks

[adnauseam]

anyone?

I'd say its right.
also
Would Cytotoxic T cells be stimulated by T Helper cells or APCs (with MHC class 1 markers) or both?
Would ct cells be found in lymph?
and
with inflammation, how does it actually help in immunity, does it have something to do with capillary permeability, or temperature, or blood flow?

[Sine]

Cell-mediated

So how does a 2nd infection response occur so fast for extracellular bacterium if no memory T-helper cells are produced?
Will we ever have to refer to memory T-helper cells(at all for VCAA) or is it sufficient to state they are "activated" by interleukin-1 produced by dendritic cells and that it activates T-cytotoxic cells to proliferate and differentiate into memory T-cytotoxic cells and active T-cytotoxic cells by secreting interleukin-2?

[Biology24123]

I'd say its right.
also
Would Cytotoxic T cells be stimulated by T Helper cells or APCs (with MHC class 1 markers) or both?
Would ct cells be found in lymph?
and
with inflammation, how does it actually help in immunity, does it have something to do with capillary permeability, or temperature, or blood flow?

T helper cell activated by APC. T helper cell activates cytotoxic T cell. Cytotoxic T cells are found in the lymph. Inflammation increases amount of phagocytes to kill pathogens and causes blood clotting

[Biology24123]

How do antibodies actually get to the site of infection if they are produced in the lymph node? Travel in the lymph fluid?

Also, do cytotoxic T cells travel in the lymph fluid to the infected cells?

[cosine]

So how does a 2nd infection response occur so fast for extracellular bacterium if no memory T-helper cells are produced?
Will we ever have to refer to memory T-helper cells(at all for VCAA) or is it sufficient to state they are "activated" by interleukin-1 produced by dendritic cells and that it activates T-cytotoxic cells to proliferate and differentiate into memory T-cytotoxic cells and active T-cytotoxic cells by secreting interleukin-2?

Why are you neglecting the humoral response in this immune response?
For VCAA, memory T cells are not required but they do certainly exist.
Say the first time a bacteria infects an organism. It will respond by producing memory B cells and plasma B cells. But this can only occur when T-helper cells are activated through APCs (phagocytes). The T-helper cells are not restricted to only B cells, and when they are activated (the t helper cells) they also proliferate into effector (the ones that will be in charge of activating) and the memory T helper cells (stored for later use). The effector T-Helper cells will then activate both B and T-cytotoxic cells to proliferate. Both of these will produce memory and effector (for B cells, it's formally known as plasma) cells. The memory cells are stored in lymph nodes or spleen for second invasion response, and the effector cells act upon the current pathogen.

The chemicals required are not necessary, as Mr. T-Rav has said before, and also the memory T cells are also not required, but they do exist.

I guess in terms of VCE biology, only memory B cells are significant. Let's just assume that naive T-helper cells and naive Cytotoxic T cells must get activated for every pathogenic invasion, and only memory B cells exist. So if a recurrence occurs, and you want the humoral response to rapidly kick in, a T-helper cell would have to encounter an APC, and this is activated. The activated will encounter one of THE MANY MEMORY B CELLS (more chance of finding one than before) which has already also internalised the antigen and presented it onto it's MHC II markers. This complex (TCR-MHC II) will activate the memory B cells to proliferate into MORE MEMORY AND PLASMA B CELLS causing an even more amplified and rapid response for the next response - which is generally why the second/third vaccinations are more effective and sought.

I guess it really depends on the context of the question, but I have never seen a VCE biol question regarding memory T cells, and I had to learn this the hard way to just relay my knowledge of memory cells onto B cells.

How do antibodies actually get to the site of infection if they are produced in the lymph node? Travel in the lymph fluid?

Also, do cytotoxic T cells travel in the lymph fluid to the infected cells?

Yes, antibodies travel in the lymph fluids and as well as the blood plasma.

Yes, cytotoxic T cells are mobile immune cells. Think of it this way, cytotoxic T cells mainly attack and destroy virally infected cells that display non-self antigens on their MHC I markers, then how would the embedded cells travel to the lymph nodes? Right, so the cytotoxic T cells must 'regulate' the body for their target cells - also think of cancerous cells, and transplanted organs, the transplanted cells would not travel to the lymph nodes, they're embedded onto the organ, so cytotoxic T cells would need to locate these themselves.

I think, not too sure though, that only inactivated B and T cells are found in the lymph nodes. Not too sure about this though, hopefully someone else can confirm it.

[cosine]

I'd say its right.
also
Would Cytotoxic T cells be stimulated by T Helper cells or APCs (with MHC class 1 markers) or both?
Would ct cells be found in lymph?
and
with inflammation, how does it actually help in immunity, does it have something to do with capillary permeability, or temperature, or blood flow?

Biology 24123 answered your other questions, but I would like to add on the last point:

Inflammation is the result of increased blood flow to the site of infection - a result of the action of histamines released by mast cells. The histamine triggers the blood vessels to vasodilate and expand, and also increases the capillary membranes, thus more blood flow is directed to the site of action. Inflammation is also a result of fever - when macrophages engulf pathogens, they release interleukin - 1 which triggers the hypothalamus to vasoconstrict blood vessels, so that heat is retained inside the organism and internal temperature increases, so that pathogenic activity is altered.

[Biology24123]

Yes, antibodies travel in the lymph fluids and as well as the blood plasma.

Yes, cytotoxic T cells are mobile immune cells. Think of it this way, cytotoxic T cells mainly attack and destroy virally infected cells that display non-self antigens on their MHC I markers, then how would the embedded cells travel to the lymph nodes? Right, so the cytotoxic T cells must 'regulate' the body for their target cells - also think of cancerous cells, and transplanted organs, the transplanted cells would not travel to the lymph nodes, they're embedded onto the organ, so cytotoxic T cells would need to locate these themselves.

I think, not too sure though, that only inactivated B and T cells are found in the lymph nodes. Not too sure about this though, hopefully someone else can confirm it.

Thanks. Hopefully someone can confirm this. So how do Ct cells actually travel to these infected cells. In the lymph fluid?

[Biology24123]

Why are you neglecting the humoral response in this immune response?
For VCAA, memory T cells are not required but they do certainly exist.
Say the first time a bacteria infects an organism. It will respond by producing memory B cells and plasma B cells. But this can only occur when T-helper cells are activated through APCs (phagocytes). The T-helper cells are not restricted to only B cells, and when they are activated (the t helper cells) they also proliferate into effector (the ones that will be in charge of activating) and the memory T helper cells (stored for later use). The effector T-Helper cells will then activate both B and T-cytotoxic cells to proliferate. Both of these will produce memory and effector (for B cells, it's formally known as plasma) cells. The memory cells are stored in lymph nodes or spleen for second invasion response, and the effector cells act upon the current pathogen.

The chemicals required are not necessary, as Mr. T-Rav has said before, and also the memory T cells are also not required, but they do exist.

I guess in terms of VCE biology, only memory B cells are significant. Let's just assume that naive T-helper cells and naive Cytotoxic T cells must get activated for every pathogenic invasion, and only memory B cells exist. So if a recurrence occurs, and you want the humoral response to rapidly kick in, a T-helper cell would have to encounter an APC, and this is activated. The activated will encounter one of THE MANY MEMORY B CELLS (more chance of finding one than before) which has already also internalised the antigen and presented it onto it's MHC II markers. This complex (TCR-MHC II) will activate the memory B cells to proliferate into MORE MEMORY AND PLASMA B CELLS causing an even more amplified and rapid response for the next response - which is generally why the second/third vaccinations are more effective and sought.

I guess it really depends on the context of the question, but I have never seen a VCE biol question regarding memory T cells, and I had to learn this the hard way to just relay my knowledge of memory cells onto B cells.

Yes, antibodies travel in the lymph fluids and as well as the blood plasma.

Yes, cytotoxic T cells are mobile immune cells. Think of it this way, cytotoxic T cells mainly attack and destroy virally infected cells that display non-self antigens on their MHC I markers, then how would the embedded cells travel to the lymph nodes? Right, so the cytotoxic T cells must 'regulate' the body for their target cells - also think of cancerous cells, and transplanted organs, the transplanted cells would not travel to the lymph nodes, they're embedded onto the organ, so cytotoxic T cells would need to locate these themselves.

I think, not too sure though, that only inactivated B and T cells are found in the lymph nodes. Not too sure about this though, hopefully someone else can confirm it.

You are really onto this immunity stuff now