(From Dr. Cain’s Handout, 30 Aug 2000, by Brian Buschman)
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Innate immunity is the body’s natural resistance to infection. It is provided by the skin, body fluids, enzymes and such.
Lymphoid organs can be “central” like the thymus and bone marrow or “peripheral” like all others. Marrow has central and peripheral functions while the thymus only has central organ functions.
Adaptive immunity is what is provided by the immune system.
Immunodeficiencies can fall into two categories:
1) Primary immune deficiencies are results of genetic or developmental failures.
2) Acquired immune deficiency diseases are results of other pathologies. They are usually secondary to another infection.
The broad family of immunoglobulin includes all forms of markers and receptors such as Ig, TCR (T-cell receptor), MHC, CD4, CD8 and so forth.
The Igs are made of two heavy chains and two light chains. IgM and IgA also have a J (joining) chain.
They have variable and constant domains. The constant domains are near the C-terminus. (i.e. C-terminus for Constant.)
The FC fragment is made up only of heavy chains and the FAB fragment is made of combinations of heavy and light chains when the Ig is cleaved with papain.
Isotypes are the classes such as IgA, IgM and so forth.
Allotypes are subclasses like IgG1, IgG2 and so forth.
Idiotypes are differences in the Ag binding region to make different Igs of the same allotype able to bind different Ags.
TCRs are antigen binding just like Ig but are bound to the plasma membrane of T-cells. There are tow classes:
1) ab-TCRs are made of one a and one b chain. They are found on T-cells of the blood and lymphoid tissue.
2) gd-TCRs are made of one g and one d chain and are found on T-cells of epithelium.
CD2 and CD3 are T-cell markers found on all human T-cells including CD4 and CD8 T-cells. That is as long as the T-cell does not have both (i.e. CD4+8+).
MHC is a cellular marker from the short arm of chromosome 6. MHC I is associated with cytotoxic T-cells (CD8 cells) and MHC II with helper T-cells (CD4 cells).
There is such a diversity of antigen recognition by Igs that the genetics must either be huge or have a complex way of combining with itself. The second is how it is done.
TCRs and Igs have parts that vary with germ-line (somatic) mutations. They are often found on chromosomes 2, 14 and 22.
Igs get most of their diversity from the combinations of genes that are used to encode for them. In one long chain of DNA there are no linear sections that code for a complete heavy or light chain. Rather in the linear path there are a number of “V-genes” (variable) followed by a number of “D-genes” (diversity) followed by many “J-genes” (joining) followed by some “C-genes” (constant). To make one heavy chain the long piece is transcribed and during post-transcriptional modification (removal of exons) all but one of each is removed. Then when translated you get a heavy chain made from one V, one D, one J and one C gene.
The light chains are made in a similar way but do not have D-genes. They will be made from one V, one J and one C. Note that the J-gene is not to be confused with the J-chain of IgM and IgA. They are two unrelated things.
Mutations also play a role in creating diversity of Igs and allowing detection of more Ags. The process is affinity maturation which involves the process by which an Ig will be changed to recognize the Ag after exposure. If the Ag is presented with IFN-g it increases the rate of affinity maturation. This makes IFN-g a useful product to put in immunizations.
Dr. Cain said that we need to memorize the following cytokines:
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