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Lecture

HTHSCI 3I03 Lecture Notes - Immunoglobulin Class Switching, Somatic Hypermutation, Cd154


Department
Health Sciences
Course Code
HTHSCI 3I03
Professor
Jonathan Bramson

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B-cell activation
Occurs in spleen and lymph nodes
CD4+ Helper T-cell
T-cell help= causes somatic hypermutation (affinity maturation) and
isotype switching
Going to get plasma cells or memory cells (i.e. maturation) following
proliferation
B-cell Antigens
Thymus dependent vs. thymus independent
Thymus dependent= T-cell help, MHCII required
o Co-stimulation (“signal 2”)= coming from the T-cells
o Protein antigens and maybe carbohydrates
o Somatic hyper-mutation (more IgG produced because remember
that the initial Ab produced is IgM), isotype switching
o Involves conventional B2 cells
Thymus independent= no T-cell required (more innate activity)
o Co-stimulation= but does not come from T-cell= TLRs Activated!!
o Carbohydrates (i.e. polysaccharides)
o Little somatic hypermutation and little isotype switching
o Therefore= less IgG than with thymus dependent
o B1 cells and marginal zone B-cells
Three outcomes of B-cell activation
Neutralization (Antibodies bind to the outside)
Opsonization (i.e. extracellular bacteria)
Classical pathway of complement activation
1) T-cell binds to B-cell
2) Triggers CD40 ligand up-regulation
3) Then CD40L on T-cell
4) IL-4 synthesis increases in the T-cell
5) Interaction causes the rearrangement of the actin skeleton= directs IL-4
directly to that space to control the amount of activation
*** Note: CD40L/CD40 interaction is IMPORTANT FOR B-CELL SURVIVAL!!
Linked Recognition
B-cells can only be recognized by T-cells that recognize the same antigen
I.e. the epitope that the T-cell receptor recognizes should be bound by the
B-cells
Steps
o Virus particle recognized by Ab and internalized by your B-cell
o Break down and present the viral proteins on MHC
o T-cell recognizes protein and activates B-cell
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