VCE Biology Question Thread

[PhoenixxFire]

Firstly, each cell displays each own unique marker on its surface (antigens)
MHC codes for a group of proteins that are found on the surface of cells and these group of proteins are able to differentiate between non-self and self antigens.

Okay so this isn't entirely correct. MHC stands for Major Histocompatability Complex. It's a protein found on the surface of all nucleated cells (so all cells except red blood cells). There are two types. MHC1 takes fragments (these are what you called antigens, they are not truly antigens, but VCAA thinks they are) of DNA that is synthesised inside the cell and holds it out into the extracellular fluid.

This is how cell mediated immunity works, Cytotoxic T(Tc) cells attempt to bind to these fragments. Tc cells have a randomly generated specificity (the shape of their binding site is random). During their development, Tc cells that can bind to fragments that are supposed to be made in that person are destroyed (if they are not destroyed, the person may have an autoimmune disease). This means that if a cytotoxic T cell binds to a fragment that is being presented on MHC1, that fragment is not supposed to be there. This means that it is there either because of cancer, a transplant, or most importantly for VCE, a viral infection. None of these things are seen as good, so the Tc cell will kill the cell presenting the fragment. It is also then stimulated to divide and differentiate and cell mediated immunity is triggered.

MHC2 is found on Antigen Presenting Cells (APC's). These are a class of immune cell that includes macrophages and dendritic cells. Macrophages and dendritic cells are also phagocytes. When they find an extracellular pathogen (e.g. a bacteria) they will engulf and destroy it. They then present the antigens that were on the pathogens surface on their own MHC2. A T helper cell will then bind to this and trigger the humoral immune response.

MHC cannot distinguish between self and non self, their only function is presenting antigens or self antigens (DNA fragments).

If a pathogen comes along, bearing non-self antigens (antigens that doesn't come from the body), then the MHC proteins on a cell (any cell?) will then identify this as foreign as it wont be able to recognize the surface antigens on the cell; thus initiating an immune response.

I've sort of explained this above, the APC (which has MHC 1 & 2) will engulf it (we don't need to know why or how they know its foreign) and then present the antigens on its MHC2. It's a T helper cell that will actually recognise it as foreign by being able to bind to the presented fragment.

If a substance comes along bearing self antigens (antigens that comes from the body) then the MHC proteins on a cell (any cell?) will be able to identify this as non-foreign as it will be able to recognize the surface antigens on the cell

As above the MHC1 will present the peptide fragments but nothing will happen because no Tc cell will be able to bind to it - they are 'recognised' as self by the lack of reaction. Also a substance won't come along with self antigens on it, the only substance with self antigens will be body cells (that's a bit of an oversimplification but you can think of it like that for VCE).

Purpose of MHC= to differentiate between non-self and self anitgens
Nature of MHC=  found on all cells?

So the purpose is to present either DNA fragments (MHC1) or antigens from pathogens (MHC2)
I've always though 'nature' question were a bit weird because I was never entirely sure what it's asking but yeah you could probably say its found on all nucleated cells, I would also mention that they're a protein found in the plasma membrane.

Let me know if any of that didn't make sense

[TheBigC]

There are two types. MHC1 takes fragments (these are what you called antigens, they are not truly antigens, but VCAA thinks they are) of DNA that is synthesised inside the cell and holds it out into the extracellular fluid.

Hey Pheonixx.

I am pretty confident that it is scientific convention to refer to self-substances as antigens as well. If you look at any immunology research papers (i.e. on ncbi) or uni texts, they are still referred to as antigens or self-antigens. It is not solely VCAA's declaration.

It is also then stimulated to divide and differentiate and cell mediated immunity is triggered.

Just to clarify (for the individual concerned), Helper T cells are necessary during this step of activation and proliferation (whereby cytokines are secreted to activate Tc cells).

MHC cannot distinguish between self and non self, their only function is presenting antigens or self antigens (DNA fragments).

Also, to clarify again. MHC is used for distinguishing between self and non-self. WIthout the MHC, this would not be possible (as presentation of antigens must occur on the MHC (as you identified)).


Other than that, great stuff Pheonixx. I hope my pedantry isn't too peeving lol.

[PhoenixxFire]

I am pretty confident that it is scientific convention to refer to self-substances as antigens as well. If you look at any immunology research papers (i.e. on ncbi) or uni texts, they are still referred to as antigens or self-antigens. It is not solely VCAA's declaration.

For sure, they’re called self antigens but they don’t cause an antibody response so they’re not really antigens.

Just to clarify (for the individual concerned), Helper T cells are necessary during this step of activation and proliferation (whereby cytokines are secreted to activate Tc cells).

I just didn’t want to try and explain immunity in response to a question about MHC haha, I couldn’t quite figure out where to cut off my explanation.

[TheBigC]

For sure, they’re called self antigens but they don’t cause an antibody response so they’re not really antigens.I just didn’t want to try and explain immunity in response to a question about MHC haha, I couldn’t quite figure out where to cut off my explanation.

Lol. Fair enough. With immunity you could babble on for days.

Also, you are right. They aren't really antigens in that sense of thought as they do not provoke an immune response* within a healthy human body. It is possible, however, that they are referred to as antigens as they provoke an immune response, though one that 'accepts' the cell as 'self'? (Vox, want to weigh in on this one with your university-level expertise?)

(*one involving the production of antibodies etc.)

EDIT: sentence clarification.

[occidit]

Lol. Fair enough. With immunity you could babble on for days.

Also, you are right. They aren't really antigens as they do not provoke an immune response* within the human body. It is possible, however, that they are referred to as antigens as they provoke an immune response,though one that 'accepts' the cell as 'self'? (Vox, want to weigh in on this one with your university-level expertise?)

(*one involving the production of antibodies etc.)

They are antigens, its just that your immune system is meticulously programmed to not have an immune response to them (look up central tolerance if you're interested).

If you put these "self-antigens" into another organism, or any T/B cells that react too strongly to them survived negative selection, they would generate an immune response

[TheBigC]

They are antigens, its just that your immune system is meticulously programmed to not have an immune response to them (look up central tolerance if you're interested).

If you put these "self-antigens" into another organism, or any T/B cells that react too strongly to them survived negative selection, they would generate an immune response

Awesome!

I was aware that they are antigens, rather the question was specifying "why" they are classified as self-antigens: which you have effectively clarified!

[Al Dem]

Thank you all so much for taking some time out of your day to help me out, I really do appreciate it!

You were completely correct in saying that I would learn more if I attempted the question first instead of just simply asking for an answer; for that I also thank you very much. You have thoroughly deepened my understanding about how the MHC works and the different classes associated within, and I am also able to correct what I previously thought was right.
I really don't know what I would do without this page and its active people

Hope you all have good fortune ahead!

[Hiea]

Hi! I was just wondering: how much ATP and NADPH does the light-dependent stage of photosynthesis result in? I've come across some conflicting it's a bit confusing.

[PhoenixxFire]

On my notes I wrote 18ATP and 12NADPH which I'm pretty sure I got from a handout my teacher gave me. I didn't cross reference that with anything though so I'm not 100% sure it's correct. I'm pretty sure that you don't need to know the exact numbers of ATP and NADPH produced in photosynthesis though, due to the way the key knowledge dot point is worded in comparison to the way the dot point about cellular respiration is worded.

[persistent_insomniac]

Hi guys could you plz help me with these questions?
1) How can cancer lead to the inhibition of apoptosis?
2) Some hormones (chemical messengers) can activate genetic material.  What benefit would this have on the target cell?
3) What stimulates hormones to be released?

Thankyou so much.

[sweetcheeks]

Hi guys could you plz help me with these questions?
1) How can cancer lead to the inhibition of apoptosis?
2) Some hormones (chemical messengers) can activate genetic material.  What benefit would this have on the target cell?
3) What stimulates hormones to be released?

Thankyou so much.

Take a shot at these yourself first. You'll learn a lot more if you try to answer the question (plus, we can see maybe where you are having trouble with these concepts).

[persistent_insomniac]

Take a shot at these yourself first. You'll learn a lot more if you try to answer the question (plus, we can see maybe where you are having trouble with these concepts).

1) I understand that decreased apoptosis can lead to cancer but I'm not sure as to how cancer can lead to stopping apoptosis? Maybe they don't respond to death ligands?
2) I have no idea.
3) A change in the body may stimulate a hormone?

[PhoenixxFire]

Hi guys could you plz help me with these questions?
1) How can cancer lead to the inhibition of apoptosis?
2) Some hormones (chemical messengers) can activate genetic material.  What benefit would this have on the target cell?
3) What stimulates hormones to be released?

Thankyou so much.

These questions aren't completely relevant for VCE, but I'll try and answer the bits I know and someone else can answer the rest.

1. My teacher told us that it can stop MHC presenting peptide fragments (or reduce the amount of MHC?), therefore stopping the cell from being recognised as cancerous, therefore it won't be apoptised.

2. The obvious example here is puberty - hormones such as testosterone and oestrogen activate genetic material which is what causes the changed during puberty. In terms of benefits I don't really know, perhaps something along the lines of allowing the cell to operate more efficiently (because it's only transcribing genetic material when it's needed).

I don't know about question 3

[darkz]

1) I understand that decreased apoptosis can lead to cancer but I'm not sure as to how cancer can lead to stopping apoptosis? Maybe they don't respond to death ligands?
2) I have no idea.
3) A change in the body may stimulate a hormone?

Q2. There are many benefits of hormones, you should just look up the most common hormones on the internet or in your textbook and you should be able to find lots of information of them, and generally all hormones regulate gene expression (i.e. activation of genetic material). In addition to the sex hormones which PhoenixxFire stated, another three really important hormones include Insulin, glucagon and thyroxine. So insulin promotes the uptake of glucose from the bloodstream (if the blood glucose level is too high so therefore it helps reduce the complications of hyperglycemia in the target cell), glucagon promotes the breaking down of glycogen into glucose which is secreted into the bloodstream (if the blood glucose level is too low) and thyroxine promotes metabolism - so you can probably conclude why its so important!

Q3. There are three ways the body can stimulate a hormone
- A change in a variable which triggers the homeostatic mechanism e.g. decrease in blood glucose levels cause the promotion of glucagon production, and the same if the blood glucose level increases, then insulin is secreted
- The hormone is secreted by stimulation by the nervous system, for example, if you feel scared or simply see something scary, then your body will produce adrenaline e.g. fight or flight theory
- The hormone secretion can be stimulated by another hormone. For example, TSH (Thyroid stimulating hormone) stimulates the thyroid to produce thyroxine

[vox nihili]

These questions aren't completely relevant for VCE, but I'll try and answer the bits I know and someone else can answer the rest.

1. My teacher told us that it can stop MHC presenting peptide fragments (or reduce the amount of MHC?), therefore stopping the cell from being recognised as cancerous, therefore it won't be apoptised.

2. The obvious example here is puberty - hormones such as testosterone and oestrogen activate genetic material which is what causes the changed during puberty. In terms of benefits I don't really know, perhaps something along the lines of allowing the cell to operate more efficiently (because it's only transcribing genetic material when it's needed).

I don't know about question 3

Q2. There are many benefits of hormones, you should just look up the most common hormones on the internet or in your textbook and you should be able to find lots of information of them, and generally all hormones regulate gene expression (i.e. activation of genetic material). In addition to the sex hormones which PhoenixxFire stated, another three really important hormones include Insulin, glucagon and thyroxine. So insulin promotes the uptake of glucose from the bloodstream (if the blood glucose level is too high so therefore it helps reduce the complications of hyperglycemia in the target cell), glucagon promotes the breaking down of glycogen into glucose which is secreted into the bloodstream (if the blood glucose level is too low) and thyroxine promotes metabolism - so you can probably conclude why its so important!

Q3. There are three ways the body can stimulate a hormone
- A change in a variable which triggers the homeostatic mechanism e.g. decrease in blood glucose levels cause the promotion of glucagon production, and the same if the blood glucose level increases, then insulin is secreted
- The hormone is secreted by stimulation by the nervous system, for example, if you feel scared or simply see something scary, then your body will produce adrenaline e.g. fight or flight theory
- The hormone secretion can be stimulated by another hormone. For example, TSH (Thyroid stimulating hormone) stimulates the thyroid to produce thyroxine

Awesome work by the two of you. These were questions that probably strayed out of the course. I think this really serves as proof positive that if you put your mind to it a bit in Biology, you can answer these questions. Definitely agree that OP should have given them a crack.



Just on Q1 to add a bit more to this: the idea that cancer can avoid apoptosis is something that is actually covered under the VCE course now. My understand is that the VCE course discusses the use of anti-apoptototic proteins. So without getting too much into the details, there are proteins in the cell that naturally inhibit apoptosis. There are also proteins that are pro-apoptotic. THe balance of these proteins almost always tends towards anti-apoptosis, otherwise cells would be dying all over. In cancer, when the cell starts to do some whacky shit, it tries to undergo apoptosis (because the cell is unsalvageable). To avoid this, the cancer will actually upregulate proteins that are anti-apoptotic, which then prevents the cell undergoing apoptosis although it really should.

Being able to avoid apoptosis is absolutely critical to a cancer cell's survival. It's one of the core components of a "successful cancer". There's actually a name for the things that are critical to cancer survival. They're called the "hallmarks of cancer". Most drugs aim to interfere with one of these hallmarks; and, indeed, just as you'd expected, there are pro-apoptotic cancer drugs that have been successful with blood cancers so far.

Last cool thing about this is that the idea that cancer needs to avoid apoptosis actually came out of Australia! Indeed, not only did it come out of Australia, but right here in Melbourne