reading: autoantibodies

[Guest guest]

I read and skimmed a decent amount about autoantibodies in states of

health, infection, and injury.

Infect rabbits with bacteria, and you can very greatly increase

their Ig reactivity to many different kinds of their own tissues.

Humans with bad burns apparantly can have autoantibodies - including

some of those autoAbs used for serodiagnosis of diseases widely

viewed as autoimmune.

If some stuff I skimmed was right, doctors who object

that " autoimmune " (one could just say inflamed) patients could be

serologically cross-reactive to say Bb, are not necessarily blowing

hot air. It seems alot of people with TB are seropositive for

syphilis without having syphilis. However, since it is easy to

examine the specificity of a given Bb serology procedure, using, for

example, TB patients, one should just do that rather than speculate

about whether lyme borreliosis resembles syphilis in this particular

regard. Im not personally aware of it having been done.

In RA, there doesnt seem to be any autoantibody for which a large

percentage of patients, from various classes of non-RA patients, do

not also have positive titers. In other words, an autoAb like

rheumatoid factor might tend to help distinguish RA from other

rheumatic diseases like lupus, yet it does not distinguish them from

burn or TB victims. Therefore, the existence of positive titers for

rheumatoid factor in alot of people with RA cannot properly have

anything at all to do with concluding RA to be an autoimmune

disease. Explicitly at least, most authors on the subject seem to be

aware of this, and in my limited experience, many RA authors are

like many MS authors in being quite clear that neither disease is

proven to be autoimmune. Yet many biologically educated people I

speak to do not have these same impressions.

In lupus (SLE), things may be different. The presence of

autoantibodies, again, is nonspecific and does not make an arguement

for an autoimmune pathology. However, anti-dsDNA Abs seem quite

sensitive and specific for SLE, according to at least one

investigation, the controls for which were unfortunately mostly RA,

with arguably not enough representation of other diseases. If a

certain kind of autoAb is in fact unique and common in SLE, this

could be taken as increasing the likelihood that SLE is a sterile

autoimmune disease. IMO a unimicrobial model could still make much

sense, but it would be somewhat harder to make a polymicrobial model

make sense - again, if in fact these data are coming out right.