This document discusses the mechanisms of humoral immunity. It describes how B cells interact with antigens through antibody production. When an antigen binds to a B cell, it forms an immune complex. This activates the B cell and causes it to proliferate and differentiate into plasma cells. The plasma cells produce antibodies that bind specifically to the antigen. Activated B cells also interact with T helper cells, which provide co-stimulatory signals to further stimulate the B cell response. The antibodies produced have various functions, including neutralization, opsonization, complement activation, and participation in hypersensitivity reactions. The primary and secondary antibody responses differ in quantity and quality.

1. Ephantus Njagi
Mechanisms of Humoral Immunity

2. Background
 Mechanisms of humoral immunity are accomplished after
interaction of:
 B cells
 Antibody production
 antigen binding

3. Interaction of antigen with B cells
 Each antibody binds to a specific antigen
similar to a lock and key through:
 Noncovalent bonds or Intermolecular forces.
 Hydrogen bonds
 Electrostatic bonds
 Van derWaal forces
 Hydrophobic bonds
 An immune complex is formed from the
integral binding of an antibody to a soluble
antigen.
 The bound antigen acting as a specific
epitope, bound to an antibody is referred to
as a singular immune complex.

4. B-cell Activation and Differentiation

5. Clonal expansion and Differentiation

6. B cells mediated immune response
Humoral immunity(HI) or antibody mediated
immunity:
The total immunological reaction that B cells recognize antigen,
then activate, proliferate, differentiate into plasma cells and
produce Ab.
 B2 cells mediated immune response toTD-Ag
 B1 cells mediated immune response toTI-Ag

7. PartⅠ: Immune response of B2 cell to TD-Ag
Characteristics ofTD-Ag:
 PossessT cell epitope and B cell epitope
 NeedTh cells participation
 Both CMI and HI
 Produce several types of antibodies: IgG
 Produce immune memory

8. 1. B cells recognize antigen
BCR directly recognize the conformational
determinant, capture Ag and present Ag signal to
Th cells
No APC , no MHC restriction
Specificity

9. conformational
linear

10. Clonal Selection
B-cells Antibody on Surface
Antigens
Only B-cells that bind antigen
are selected

11. Clonal Expansion
B-cells Antibody on Surface Proliferation of selected
B-cell

12. Somatic Mutation
B-cells Antibody on Surface Improved Antibody Binding
By Genetic Rearrangement
Somatic
Mutation

13. 2. B cells activation, proliferation and
differentiation
(1) B cell activation: double signals
 First signal : antigen signal
BCR--conformational determinant on the surface of Ag
Igα/Igβtransduct first signal
CD19/CD21 (co-receptor) binds to C3d on Ag
 Second signal: co-stimulatory signal
The CD40 on B cells binds to CD40L on activatedT cells

14. CD40
Immunoglobulin
receptor
MHC II
Antigen
Cytokine
receptor
B
cell
B7
B7 CD28
TCR
TCR
T helper
cell
1. Antigen presentation to
Th cell
2. B7 expressed
B
cell
3. Th cell is
activated
and expresses
CD40 ligand,
Cytokines
secreted
CD40
ligand
Cytokine
B
cell
T helper
cell
B
cell
B
cell
B
cell
5. B cell activated
6. B cells proliferate, differentiate, secrete Ig

15. Interaction between Th cell and B
cell
 B cells act onT helper cells:
 B cells present Ag toTh cells
 B cells provide B7 forTh cells
 T helper cells act on B cells:
 ActivatedTh cells provide co-stimulatory molecule for B cells:
CD40L-D40
 ActivatedTh produce Cytokines to help B cells proliferate and
differentiate
 Activated B cells express receptors of cytokines
 ActivatedTh2 secrete cytokines IL-4, IL-5, IL-6 to enhance
proliferation and differentiation of B cells
 B cells differentiate into plasma cells (antibody forming cells)-
produce Ab, some activated B cells become memory B cells

16. Interactions between B cell and Th cell
B cell
activation
B cell Th cell
Ag processing
Th cell
activation

17. Cytokines affect proliferation and
Class switch of B cells

20. 3. Stage of effect----the function of Ab
1. Neutralization-Ab covers up sites on toxic molecule/virus.
2. Opsonization-Ab-mediated phagocytosis.
3. Complement fixation-cascade reacts to ag-ab complexes.
4. Agglutination/precipitation-Cross-link ags into
complexes-aids phagocytosis.
5. Immobilization-Abs bind to flagella etc. & prevent escape
macrophage death.
6. ADCC-NK, macrophage
7. Participate in hypersensitivity-I,II,III

21. 1. Neutralization:
* to neutralize microbial toxins and animal venoms
* to prevent viruses and bacteria from infecting cells

22. 2. ADCC—NK
Antibody-coated target cells can be killed by natural killer cells(NK cell) in
antibody-dependent cell-mediated cytotoxicity, that is called ADCC.

23. 3.Opsonization – macrophage
Fc receptors on phagocytes trigger the uptake of antibody-coated bacteria.
As a result, this action enhance phagocytosis of the bacterium.

24. Complement proteins bind to antibodies.
4.Activation of complement
Complement can be activated to directly lyse bacteria by the presence of
antibodies bound to the bacteria.

25. 5. Participate in hypersensitivity
IgE binds to high-affinity Fc receptors on mast cells and basophils, and leads to
the rapid release of granules containing inflammatory mediators into
surrounding tissue, cause hypersensitivity

30. Primary and secondary antibody responses to protein
antigens differ qualitatively and quantitatively