Antibody concepts - (Jun/09/2007 )

Good luck from me aswell biology_06er. My answers are pitched at university level so you can probably ignore some of the detail. I'm not sure I had a great grasp of this stuff back in uni. either. What you said is correct there are multiple gene segments for V, D, J, etc. and one segment for each of these is combined together with the constant region. Multiplying by the number of gene segments to account for all the combinations of V-J and J-D-J and different combinations of heavy and light chains together accounts for the diversity of BCRs.

Antibody structure is 2 heavy chains and 2 light chains (kappa or lambda). The variable regions of both chains are in the antigen binding region. The antibody genes have multiple gene segments (V-J for light chains and V-D-J for heavy chains) making up the variable regions. Only one possible combination per cell occurs joining these segments randomly by recombination. This determines the variable region and the antibody/B cell receptor specificity. (The joining can be imprecise and nucleotides may be added plus there somatic mutation of antibody genes which is enzyme driven. This increases the diversity.)

Your question/answer about the hypervariable loops/regions (also called complementarity-determining regions, CDRs) seems about right. The amino acids within the variable region that contacts/binds the antigen are more variable if you look at a lot of different antibody sequences than the areas around them. So the areas around the hypervariable loops are more to form the overall structure of the antibody which is the same for each subclass and the hypervariable parts bind the antigen and there are different/more variable in different antibodies. I had to go back to the textbook more for this one and it difn't say how this variability is brought about but part of it must be in the different gene segments and maybe some of the other mechanisms are involved too. Not much help I know.

There should be some diagrams in Janeway to help with this.
MHC is on the cell surface but it gets loaded with peptide it presents within the cell before going onto the cell membrane and presenting it.

Good luck,
Ceri

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so just to let you know how exam went...hmm alright one if the essays i did on genetics was completely **** but I just hoped I passed! anyway i just wanna check a few of my MCQ'S to see if i was right-the bold answer is what i chose

1) which of the following cell surface molecules is expressed by human CTL, and allows them to specifically recognise virus-infected cells and cancer cells?

CD8
T cell receptor
MHC class I
CD4

2) The clonal selection theory implies that:

antigens activate specific lymphocytes
the body selects which antigens it will respond to
memory cells are present at birth
related people have similar immune responses

3) which of the following is NOT true about helper T cells

they bear surface CD4 molecules
they function in both humoral and cell-mediated immune responses
they recognize polyssaccharide fragments presented by class II MHC molecules
when activated, they secrete cytokines

4) the father is Rh- and the mother is Rh+. they have had three children without adverse problems due to the Rh factor. the mother is pregnant again. In terms of the Rh factor, the risk to the fetus within the uterus:-

is less than before
is greater than before
is the same and remains relatively moderate
never was a problem

and incase ure interested the immune essay question was: is the repertoire of the immune system limited by the atomic structure of antogen receptor molecules? Describe the antigen presenting binding molecules on the surface of lymphocytes and antgen presenting cells, and discuss the origin of the diversity of antigen binding specificities of these molecules
..I talked about the structure of MHC/antibodies like light/heavy chains..alpha/beta domains and then went onto talk about the vdj regions--do you guys reckon this will be ok?

again thanks for all your help!!

biology_06er

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. . .. oops. Think about this again!

Let's give biology_06er one more chance in forum. . .. ssssshhhhhhhhhhh everyone.

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so i take it the other ones are right??

ok so for that question..the reason for my answer (and i was really unsure about this question cos i hadn't read anything about this before hand) was that during one lab one day i thoought i remembered hearing that after a certain # of children you might have problems with the next child...but if this is wrong then is it "is the same and remains moderate" seeing as the 3 children before were fine...

biology_06er

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Don't worry about the number of children. Just see how immunology will act on mother and how it will act on the fetus.

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ok well after having a quick look online I read that a problem only arises if he father is Rh+ and the mother is Rh-. Basically
If the mother conceives a child who is RH+ the womans body may make antibodies that attack future Rh+ offspring.

But if mother is Rh+ and they have a Rh- baby it doesn't matter because the RBC'S of the baby do not have the surface antigen hence the mother does not find it as foreign hence it doesn't make antibodies and the answer is 'never was a problem'...

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So, I have a question now.

Child is Rh Neg and mother is Rh Pos; then will the child develop Ab against Rh Antigen?

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umm I'm thinking yes

Reason:
Because from the baby's point of view the mother has foreign antigens on her RBC cell membrane and the baby finds this foreign ie makes antibodies??

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Yes, the reason being that. But, will the baby do so?

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I know the answer, but I will let our enthusiastic biology student find the answer. She is mature enough

About the other questions, I don't think this answer is right:

As a matter of fact, the main role of helper T-cells is to modulate other lymphocytes activity, so they are continuously secreting one or another cytokine when active.

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