VCE Biology Question Thread

[vox nihili]

For T cells to be activated, they must bind to an antigen on a MHC marker. There are two types of markers, class I and class II. Class II are on macrophages and B cells (antigen presenting cells). Class I are on any cell with a nucleus. When a virus infects a cell, the cell may present epitopes on its class I MHC markers. Do T cells only bind to class II markers on antigen presenting cells to be activated? Or can they bind to class I markers on any cell to be activated? Sorry if this question is confusing.

Helper T-cells bind to class II
Cytotoxic T-cells bind to class I

[ALE0017]

Hey Guys,
I have Biology Sac on Monday and I have no clue what's going on? Its on meiosis. And the we can present it in any way we can and the rubric says
An explanation of each phase during meiosis i.e. interphase, prophase, metaphase, anaphase, telophase and cytokinesis (I and II)
The inclusion and explanation of the cell cycle
Explanation of crossing over and independent assortment.
Any help appreciated?
Thanks

[plsbegentle]

Hey Guys,
I have Biology Sac on Monday and I have no clue what's going on? Its on meiosis. And the we can present it in any way we can and the rubric says
An explanation of each phase during meiosis i.e. interphase, prophase, metaphase, anaphase, telophase and cytokinesis (I and II)
The inclusion and explanation of the cell cycle
Explanation of crossing over and independent assortment.
Any help appreciated?
Thanks

tbh, this should all be in your textbook... maybe have a look through it first and if there's still any questions, ask away!

[cosine]

Hey Guys,
I have Biology Sac on Monday and I have no clue what's going on? Its on meiosis. And the we can present it in any way we can and the rubric says
An explanation of each phase during meiosis i.e. interphase, prophase, metaphase, anaphase, telophase and cytokinesis (I and II)
The inclusion and explanation of the cell cycle
Explanation of crossing over and independent assortment.
Any help appreciated?
Thanks

Meiosis has two major stages: Meiosis I and II

Meiosis I:
Interphase: DNA of the diploid germ-line cell replicates and as per normal of mitosis.
Prophase I: Nuclear membrane disintegrates, chromatin condenses into chromosomes and spindle fibres form as the centrioles move to opposite poles.
Metaphase I: The homologous chromosomes line up at the equatorial plate (mitotic plate) with the aid of the spindle fibres. The kinetochore spindle fibres attach to each kinetochore section on each chromosome.
Anaphase I: The homologous chromosomes are separated to opposite poles of the two daughter cells (not identical since chromosomes were homologous, one from mother and one from father)
Telophase I: The nuclear membrane starts to reform over the chromosomes and cytokinesis starts. Chromosomes turn into chromatin again.
Cytokinesis I: The two daughter cells pinch off. (Two haploid cells but they both have chromosomes with sister chromatids, hence they have 23 chromosomes, but 46 DNA molecules in the nucleus)

Meiosis II:
NO Interphase, hence no DNA replication!
Metaphase II: The chromosomes line up at the equatorial plate (mitotic plate) with the aid of the spindle fibres. The kinetochore spindle fibres attach to each kinetochore section on each chromosome.
Anaphase II: The chromatids are separated to opposite poles of the four daughter cells. Hence all chromosomes are now singular (non-sister chromatids)
Telophase II: The nuclear membrane starts to reform over the chromosomes and cytokinesis starts. Chromosomes turn into chromatin again.
Cytokinesis II: The four haploid gametes are formed (in females, only 1 survives this process).

[chickennugget]

When describing the humoral response, is it necessary to describe how T helper cells bind to antigen presenting cells via MHC markers to produce cytokines that lead to the division of B cells?

[cosine]

When describing the humoral response, is it necessary to describe how T helper cells bind to antigen presenting cells via MHC markers to produce cytokines that lead to the division of B cells?

That statement is not 100% true. Activated T helper cells must travel to lymph nodes to meet a complementary B cell that has already encountered and engulfed the specific antigen, and presented it onto it's MHC II markers. Only when the T helper cell binds to the MHC II marker with the antigen, only then will it release chemicals to induce proliferation. Yes, this is important in stating as its the mechanism by which B cells undergo division into plasma and memory cells

[chickennugget]

That statement is not 100% true. Activated T helper cells must travel to lymph nodes to meet a complementary B cell that has already encountered and engulfed the specific antigen, and presented it onto it's MHC II markers. Only when the T helper cell binds to the MHC II marker with the antigen, only then will it release chemicals to induce proliferation. Yes, this is important in stating as its the mechanism by which B cells undergo division into plasma and memory cells

Is it okay (when describing JUST the humoral response) something like "cytokines from T helper cells assist the B cell to divide into plasma and memory cells"? Or do I have to mention the things about MHC markers?

[vox nihili]

Is it okay (when describing JUST the humoral response) something like "cytokines from T helper cells assist the B cell to divide into plasma and memory cells"? Or do I have to mention the things about MHC markers?

Certainly in VCE that's completely fine. Even at later stages that'd probably suffice too if there are any early year uni students floating around

[sweetcheeks]

Is this acceptable for an immunisation response for a specific virus?

The person is injected with a sample of antigens of the virus. Macrophages detect as foreign and engulf and present the antigens on its surface.
T helper cell detects these antigens and release cytokines, some of which cause B cells to replicate more (to increase diversity of antibodies).
When the correct B cell with the specific antibody is produced it replicates and differentiates into B plasma cells and B memory cells.
When a subsequent infection of the virus reenters the body, the memory B cells detect and respond to it with a swift and high response.

I know that there is a lot more (T helpers have to detect the correct B cell to cause it to differentiate/replicate) to it but is that sufficient for VCE?

[cosine]

Is this acceptable for an immunisation response for a specific virus?

The person is injected with a sample of antigens of the virus. Macrophages detect as foreign and engulf and present the antigens on its surface.
T helper cell detects these antigens and release cytokines, some of which cause B cells to replicate more (to increase diversity of antibodies).
When the correct B cell with the specific antibody is produced it replicates and differentiates into B plasma cells and B memory cells.
When a subsequent infection of the virus reenters the body, the memory B cells detect and respond to it with a swift and high response.

I know that there is a lot more (T helpers have to detect the correct B cell to cause it to differentiate/replicate) to it but is that sufficient for VCE?

Its very good, but instead of saying that the macrophages present the antigens on its surface, say they present them on their MHC II markers, both are correct, but the latter is more appropriate and specific.

Also, what do you mean by 'When the correct B cell with the specific antibody is produced'?

[sweetcheeks]

What I'm referring to is the process of clonal selection. When the B cell that has the correct antibody for the antigen is made and it binds to the antigen (usually along with help from helper T), it causes it to rapidly proliferate and differentiate.

[chickennugget]

Why does injecting antigens into someone who has allergies beneficial? I thought this would cause an immune response, making the situation worse?

[sweetcheeks]

Why does injecting antigens into someone who has allergies beneficial? I thought this would cause an immune response, making the situation worse?

It does cause an immune response, but a little bit different than the allergy response. The allergy response is due to the production to IgE antibodies and them attaching to mast cells. Injecting someone with the antigens attempts to stimulate the immune system to produce IgG (I think) antibodies (an subsequently B memory cells)  which will respond and neutralise, without causing an allergy response, before the mast cells can detect and respond themselves. The production of IgE/hypersensitivity appears to be a sort of malfunction and usually shouldn't occur.

[cosine]

What I'm referring to is the process of clonal selection. When the B cell that has the correct antibody for the antigen is made and it binds to the antigen (usually along with help from helper T), it causes it to rapidly proliferate and differentiate.

Yes that is correct, perfectly fine. 

Why does injecting antigens into someone who has allergies beneficial? I thought this would cause an immune response, making the situation worse?

That is true, injecting antigens into someone who has allergies is not beneficial because upon the first injection, the stimulation is the increased amount of B cell production, hence more antibodies are secreted and more mast cells are produced (since antibodies are embedded onto the mast cells). Because there are more B memory cells, then the second invasion of this antigen will cause a more intense and hypersensitive response, as the B cells will detect the antigen more quickly with more of an efficient response, and hence more antibodies will be secreted and bound on the membrane of mast cells, leading to degranulation of histamine upon antigen-antibody binding on mast cells. Usually you would want more memory B cells to fight off antigens more quickly upon second invasion, but with allergies, its not always the case. So yes, it will make it worse for the person.

[cosine]

It does cause an immune response, but a little bit different than the allergy response. The allergy response is due to the production to IgE antibodies and them attaching to mast cells. Injecting someone with the antigens attempts to stimulate the immune system to produce IgG (I think) antibodies (an subsequently B memory cells)  which will respond and neutralise, without causing an allergy response, before the mast cells can detect and respond themselves. The production of IgE/hypersensitivity appears to be a sort of malfunction and usually shouldn't occur.

Not always the case, think about when the antigen occurs naturally through intake of an allergic particle, why would there still be an allergic reaction if no IgE antibodies are produced? Thing is, different B cells produce different antibodies, very complex process/differentiation - not required for VCE