Humoral Immunity

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Humoral Immunity

Antibodies in the body's "humors" (blood, lymph) provide defense

Antibodies target bacteria & free viruses and mark them for destruction by phagocytes or complement of nonspecific/innate immune system

Antibodies (Abs)

Immunoglobulins (Igs)

Secreted by activated B cells called plasma cells

Antibody Structure

Y-shaped

4 polypeptide chains:
- 2 light + 2 heavy chains bound together by disulfide bonds (S-S)
- Each polypeptide has variable and constant region

Variable regions = antigen binding site

Constant regions
- 5 different constant regions of heavy chains => form 5 different stems
- Different stems define 5 different classes of Ab's:
IgM, A, D, G, E
- Sites for complement and macrophage binding
- Sites for binding to cells (B cells, basophils)

IgM

Monomer (1) binds to B cells to act as an Ag receptor for B cells; Pentamer (5) circulates and is first class released during a primary response; Potent agglutinator; Complement fixation

IgA

Found in body secretions; prevents attachment of Ag to epithelial cell surfaces

IgD

Binds to B cells to act as an antigen receptor for the B cells

IgG

Main Ab for primary and secondary immune responses; protection against pathogens circulating in blood and lymph; Complement fixation; Crosses placenta (passive immunity)

IgE

Binds to basophils causing the release of histamine when triggered by an Ag (allergic reactions)

4 Mechanisms of Antibody Action

1. Neutralization
2. Agglutination
3. Precipitation
4. Complement

Note: Ab's do NOT destroy antigen directly; Ab's mark antigens for destruction by other parts of the immune system

Neutralization

Ab's bind to and block specific sites on Ag's

- Prevents Ag's from binding to cells - cannot cause injury to cells

- Enhances phagocytosis

Agglutination

Ab's bind to numerous cell-bound Ag's (cross-linked)
- Crosslinking causes clumping
- Enhances phagocytosis
- IgM - potent agglutinator because pentimeric form has many sites for binding to Ag (causes agglutination in positive blood typing reactions)

Precipitation

Soluble Ag's are cross-linked with Ab's
- Insoluble complexes formed
- Enhances phagocytosis

Complement Activation (classical pathway)

(Main mechanism used against cellular Ag's)
Complement: inactive group of proteins in blood plasma that are activated when Ag/Ab complex forms
Binding of complement to Ag/Ab complex (complement fixation)
- Cell lysis by MAC
- Enhances inflammation (chemicals released)
- Enhances phagocytosis (opsonization)

B Cell Activation & Clonal Selection

When a B lymphocyte is exposed to Ag:
1. B cell binds to Ag
2. Causes activation of B cell
3. Triggers clonal selection: proliferation of B cell to make more B cells that have the same receptors (clones)

Clonal Selection & Differentiation of B Cells

Most B cells turn into Plasma Cells
- Produce Ab's against specific Ag
(2000 molecules per second)

Some B cells become Memory B Cells
- Inactive; hang out in lymphoid tissues

Primary

1st exposure to Ag
- Takes about 5 days to mount an attack
- Peak levels of Ab's in 10 days and then decline

Secondary

Memory B cells respond to re-exposure to the same Ag
- Ab production is faster (peak levels in 2-3 days), higher, more prolonged (weeks to months)

Humoral Immune Response Attacks EXTRACELLULAR Ag's

B cells & Ab's in blood & lymph:
- Bind extracellular Ag's that are present in their natural state
- CANNOT bind intracellular Ag's

Intracellular Ag's include:
- Endogenous antigens (synthesized by body cells)
Viral proteins synthesized by virus-infected cells
Non-normal (mutated) proteins produced by body cells that become cancerous.
- Exogenous antigens- extracellular antigens that have been engulfed and broken down in phagolysosomes

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