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gwa, I don’t know much about alpha B crystallin except that it’s a major protein in the lens of the eye and has been proposed as an auto-antigen in MS. Many proteins have been posited as auto-antigens in MS, including Myelin Oligodendrocyte Glycoprotein and a number of Heat Shock Proteins and others. In fact alpha B crystellin is itself a member of the small-HSP family. The fact that there are such a plethora of potential ‘auto-antigens’ casts doubt on the whole auto-immune theory. Occam’s razor suggests that they are all likely to be secondary; indeed, a covert chronic infection with an intracellular pathogen would disarrange a number of host systems. And in fact this has been shown; antibodies to C. pneumoniae specific HSP60 have been found in the CSF of persons with MS. Bacterial HSP60 is upregulated in persistent infection and is highly antigenic; the antibodies so produced may act against mammalian analogues. This has been termed molecular mimicry. HSPs are good candidates for this because they are highly conserved. Interestingly, most bacteria possess genes for alpha crystallins, though apparently not chlamydiae..

One other factor is that chronic infections with C. pneumoniae breach the blood-brain barrier; in addition macrophage / microglia cell types are very actively motile and it’s conceivable that they transfer proteins to places where they are not normally found. C. pneumoniae causes eye infections, including uveitis, retinal vasculitis and macular degeneration, and associated inflammation may break down the barrier between eye and CNS.

As far as I can see, the presence of alpha B crystallin is found in the CSF in a number of neurological conditions and is not specifically found in MS. I know very little about this, but to speculate on its being an autoantigen would mean that you would have to buy into an autoimmune theory; evidence supporting primary autoimmunity is looking increasingly shaky. The fact that carriers of a certain rare genotype of alpha B crystallin have a particular variant of MS (with a non-inflammatory, rapidly neurodegenerative course) doesn’t detract from the idea of a primary chronic infection. Many chronic infections (such as TB and leprosy) take on a particular clinical appearance depending upon the host’s genetic inheritance.