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March 28, 2024, 09:45:13 pm

Author Topic: VCE Biology Question Thread  (Read 3570414 times)  Share 

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grannysmith

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Re: VCE Biology Question Thread
« Reply #1965 on: June 15, 2014, 08:57:08 pm »
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When exactly is a B cell "activated"? Is it when they bind to an antigen specific to its Ig, or when helper T cells release interleukin-2, which stimulate their proliferation and differentiation?

grannysmith

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Re: VCE Biology Question Thread
« Reply #1966 on: June 15, 2014, 09:02:34 pm »
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Considering lymphocytes are antigen presenting, couldn't they express viral antigen fragments on both MHC I and MHC II molecules?
Also, are T- and B-lymphocytes phagocytic, considering that they're APCs?
Perhaps antigen fragments bound to MHC II signals that the cell is infected, whereas those bound to MHC II are essentially fulfilling their roles as APCs, attracting appropriate helper T cells?

I think they are phagocytic, as B cells which bind to antigens specific to their receptors must engulf them, break them down into fragments and express them on their MHC II to attract the appropriate helper T cell. I just don't know when exactly the B cell is activated?

nhmn0301

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Re: VCE Biology Question Thread
« Reply #1967 on: June 15, 2014, 09:03:37 pm »
+1
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?
Correct me if I'm wrong here:
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.
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katiesaliba

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Re: VCE Biology Question Thread
« Reply #1968 on: June 15, 2014, 09:07:17 pm »
+2
When exactly is a B cell "activated"? Is it when they bind to an antigen specific to its Ig, or when helper T cells release interleukin-2, which stimulate their proliferation and differentiation?

I'm pretty sure that MOST B-cells require interleukin-2 as well as the binding to their complementary antigen in order to become activated. That's what my TSFX notes say anyway  ::)
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grannysmith

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Re: VCE Biology Question Thread
« Reply #1969 on: June 15, 2014, 09:17:22 pm »
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Correct me if I'm wrong here:
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.

Right, that makes sense. I've read somewhere that memory cells can differentiate directly into plasma cells, without the need of helper T cells? So they're essentially primed to secrete antibodies. 
But yes, the secondary immune response is quicker as there is a greater number of memory cells specific to the pathogen, and hence a greater and faster production of antibodies.

nhmn0301

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Re: VCE Biology Question Thread
« Reply #1970 on: June 15, 2014, 09:18:04 pm »
+1
When exactly is a B cell "activated"? Is it when they bind to an antigen specific to its Ig, or when helper T cells release interleukin-2, which stimulate their proliferation and differentiation?
B cells can be activated by both. These are also be called T-cell dependent and T-cell independent activation (you don't need to know the specific name).
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grannysmith

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Re: VCE Biology Question Thread
« Reply #1971 on: June 15, 2014, 09:21:38 pm »
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B cells can be activated by both. These are also be called T-cell dependent and T-cell independent activation (you don't need to know the specific name).
Yeah, but would we have to mention T-helper cells when describing the humoral response - considering that there is both dependent and independent activation? I suppose so, just to err on the side of caution :)

simpak

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Re: VCE Biology Question Thread
« Reply #1972 on: June 15, 2014, 09:24:16 pm »
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To clarify from the above the 'activation by both' - you can't really activate a B cell (for the purposes of VCE) with cytokines alone. The B cell can be activated by both in combination (usually) or by antigen alone (T cell independent activation) in rare cases.
The term activation in the case of T cell dependent activation would refer to both steps - antigen recognition and cytokine reception - and activation would not be complete until both have occurred.

You should mention T cells when describing the humoral response irrespective of their being two circumstances - the classical model is that Th cells should be required for proper B cell activation. The lack of Th cell help is a rarity and therefore not what your examiner would be looking for if you're required to answer a question on how the humoral immune system becomes active.
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grannysmith

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Re: VCE Biology Question Thread
« Reply #1973 on: June 15, 2014, 09:40:26 pm »
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Thanks for that, simpak.

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?
« Last Edit: June 15, 2014, 09:42:47 pm by grannysmith »

simpak

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Re: VCE Biology Question Thread
« Reply #1974 on: June 15, 2014, 09:43:19 pm »
+1
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 :)
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grannysmith

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Re: VCE Biology Question Thread
« Reply #1975 on: June 15, 2014, 09:46:45 pm »
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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 :)

So the MHC I marker of the cancerous cell effectively becomes an antigen?

simpak

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Re: VCE Biology Question Thread
« Reply #1976 on: June 15, 2014, 09:51:38 pm »
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So the MHC I marker of the cancerous cell effectively becomes an antigen?

No, 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?
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grannysmith

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Re: VCE Biology Question Thread
« Reply #1977 on: June 15, 2014, 10:15:58 pm »
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Yep that makes perfect sense! Thanks.
« Last Edit: June 15, 2014, 10:18:25 pm by grannysmith »

simpak

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Re: VCE Biology Question Thread
« Reply #1978 on: June 15, 2014, 10:18:33 pm »
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Unsure - I think it would be good to know that cancer cells can be killed by CTL but perhaps you don't need to know the mechanisms behind it :)
I'm so far distanced from the VCE study design now haha.  I just think that it can be easier to answer peoples questions even if they are beyond the study design otherwise they get confused with stuff that is actually on the study design.
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RazzMeTazz

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Re: VCE Biology Question Thread
« Reply #1979 on: June 16, 2014, 12:11:35 am »
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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?