Notes April 24

V. Classes of antibody= isotypes

*Different isotype properties because of different heavy chains and different Fc regions

a. IgG
*Most common isotype found in blood
Binds very avidly to antigens (more so than other types)
*Free antibody: not attached to cell surface
*IgG is transported across placenta (can also be in breast milk & anti-venom)

Passive Immunity: “Acquired” immunity to pathogen from pre-formed antibody from someone else

b. IgM
*Forms pentamers
*Not bind as avidly as IgG individually (but binding sites work together in pentamer to increase binding avidity)
*As a flat molecule IgM pentamer not bound by C1
*But when bound to microbe, makes a “tent” allows C1 to bind
*First isotype of antibody to be secreted by B-cell
*IgM bound to B-cell surface= receptor part of B-cell receptor

c. IgE ->Mast cell, eosinophil degranulation
eosinophils contain antimicrobial properties & mast cells contain inflammatory mediators (such as histamine)
*Histamine -> brochoconstriction
-> mucus secretion

VI. Immunopathology: Types of hypersensitivity reactions

a. Type I
*Ex. Allergies, Asthma
*IgE against wrong target

*Allergies higher in “clean” environment because we don’t get enough exposure to parasites = Hygiene Hypothesis

*T-cell-independent antibody response= B1, marginal zone B-cells spontaneously producing nonspecific antibody

T-cell dependent:
*Antibody production induced by T-cell receptor presenting antigen to B-cell in secondary lymphoid tissues
-> Relies on clonal expansion T-cells

*Like in T-cell rec., IgM-antigen binding a result of VDJ recombination.

*T-cell presents antigen to B-cell receptor
-> Prolonged contact
->Somatic hypermutation

Somatic hypermutation
*Cytidine deaminases convert Cytosine into Uracil
*Here , act on V segment of gene that’s coding for this particular B-cell receptor
*V= Variability
*So very high rate of random mutation in V segment
*Tweaked B-cell receptor then expressed on B-cell
*Somatic hypermutation of B-cell receptor-> more perfect match
*This results in “perfect fit” antibodies being secreted by B-cells
*Since IgM secreted first, it binds less well to antigen
*Then, heavy chain gene expression changes – this equal isotype switching

*Mainly IgG secreted

*Plasma cells can live > several years
*Plasma cell= terminally – differentiated B-cell secreting lots of antibody
*Plasma cell maintenance differentiation because of IL-6.
*Some perfect fit B-cells don’t become plasma cells, don’t secrete antibody = memory B-cells that can live for decades

*Upon re-exposure to matching antigen, memory B-cells clonally expand, differentiate into plasma cells.

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