Molecular Mimicry theory and hereditary predisposition
[QUOTE=DavidBod]Norb. CIDP does not show abnormal genes it is not a genetic disorder, it is acquired though at present, while we know the triggers in about 50% of GBS the triggers for CIDP are unknown. DocDavid[/QUOTE]
DocDavid, I was referring to one of the more popular theories of the underlying mechanics of auto-immune diseases, molecular mimicry, which according to some scientists includes a hereditary predisposition – but not a genetic defect. I just found an interesting write-up at “www.mult-sclerosis.org/MolecularMimicry.html”.
The genetic connection is not mentioned there directly. Here is the way I understand it: T-Helper cells have receptors called HLA which are the ones presenting parts of an antigen and – if a match is found – activate an immune response. Some antigens may have a stretch of amino-acids identical to a part of the myelin. This triggers the auto-immune reaction. Hepatits B has been found to be one of those antigens (Fujinami and Oldstone at Scripps Research Institute). Now, fortunately most people do not get this kind of reaction. The reason is that HLA molecules are different from person to person, a normal variation and not a genetic flaw.
L. Steinman explains in an article on auto-immune diseases (“Life, Death and the Immune System”) why not everybody mounts an immune response to myelin basic protein and develops MS (as an example – my comment): “The reason seems to rest for the most part with the differences in individuals’ HLA types. The HLA molecule determines exactly which fragments of a pathogen are displayed on the cell surface for presentation to T cells. One individual’s HLA structure may bind a self-mimicking fragment and present it to the immune system, whereas another’s may bind a fragment unique to the pathogen that does not mimick self. In the latter case, the pathogen is attacked, but self-tolerance is not violated.”
Here the graph which follows this paragraph.