Antibodies in infection

Question 1

Lymphocyte subpopulations

• effector responses and regulatory responses

Answer 1

Effector responses

B cells: Produce antibodies
T cells: Become antigen-specific cytotoxic cells
Natrual killer cells: release short range cytotoxic factors

Regulatory responses

Cytokine release

CD4 T helper lymphocytes

Question 2

Lymphocyte activation

T cells vs B cells

Answer 2

B cells

Activation of B cells occurs when an antigen arrives in the lymph nodes (On antigen presenting cells, or viral/bacterial surface) and the antigen comes into contact with a B cell receptor that has affinity for this shape. The B cell receptor is a surface immunoglobulin, it resembles the free antibodies that it produces, except the Fc region is stuck to the B cell. It associates with the transmembrane protein CD79 which tranduces changes in the SIg into internal signalling within the B cell. This causes the B cell to differentiate and proliferature (into memory cells and antibody-producing cells).

T cells

Similarly, once in contact with a completementary antigen in the lymph nodes, activation of T cells will occur. The T-cell has a T-cell receptor by which is senses this antigen, which is a glycoprotein. It is associated with the transmembrane protein CD3 which acts to transduce conformational changes upon binding into internal cell signalling pathways. Causes the T cell to then differentiate and prolfierate into either cytotoxic or helper cells.

Question 3

Affinity

2 consequences of this

Answer 3

Receptors for antigens can have high, medium, low, or no affinity.

Consequence 1: I tmeans that not every antibody has to perfectly bind to only 1 antigen. This type of absolute specificity would require a massive repitoire of antibodies and receptors. This way it means that our still huge bu tlimited repitoire of receptors is enough for the myriad of pathogens the immune system will encounter.

Consequence 2: Since you can technically have one antibody that can react to multiple different things, it increases the risk of cross-reactivity.

Question 4

Antibody structure

Answer 4

Question 5

Presence of foetal antibodies during development and post-natally.

Answer 5

Antibodies in the foetus increase exponentially during development. This is because the antibodies of the mother can cross the placenta and enter the baby. So the baby is protected by mothers antigens.

Following birth, since these antibodies are broken down, the maternal antiody count in the baby will drip despite the mother still supplying antibodie sthrough brest milk. But at about 2 months postnatally the baby will begin to make its own antibodies. (6 months, enough self production of antibodies to start enquiring about vaccinations)

Question 7

B cell clonal activation

Answer 7

Once the B cell binds to an antigen with decent affinity using SIg, it becomes activated and causes the B cell receptor changes. These changes are dependent on helper signals from other cells within the lymph node, which allow the complete activation of the B cell.

Once this has been achieved, the B cells will proliferate and differentiate, either into plasma sells which secrete antibodies or memory cells.

memory cells require less helper signals to become activated and respond faster - basis of vaccination.

Question 8

Antibody effector mechanisms

Answer 8

Neutralisation

This is when antibodies recognize for example the surface proteins of a virus, and will coat the entire virus. This prevents the virus from being able to come into contact with host cells and infect them

Opsinization

Antibodies will coat a bacterium or virus, and then the Fc region on the antibody allows for an immune cell to bind and initiate phagocytosis. it effectively enhances the phagocytotic ability of neutrophils/macrophages.

Antibody-dependent cellular cytotoxicity

NK cells are able to bind the Fc region of antibodies that have bound to a pathogen. This stimulates the natural killer cells to release short range toxic factors to kill the pathogen.

Complement activation

when the antibody is free floating its arms are positioned so that the structure of the antibody is like a T. But once the antibody arms have bound it becomes Y shaped and this opens up the Cd2 (complement domain). This allows the activation of complement, which in turn allows the formation of chemotaxtic gradients, vascular changes, opsinisation, and formation of the membrane attack complex. This is the classical pathway for activating complement.