KROONINEN INFEKTIO AUTOIMMUUNIREAKTION YLLÄPITÄJÄ?

[Bb]

Lähettäjä: Soijuv Lähetetty: 3.3.2005 10:31

Yhden lääkärin vastine edelliseen artikkeliin. Hänen (monien muidenkin) mukaan borrelioosin yhteydessä tavattujen autoimmuunisairauksien syynä saattaa olla jatkuva infektio jonka vuoksi autoimuunireaktiot eivät "sammu".


Molecular mimicry as a possible mechanism of disease in chronic Lyme disease is being revealed more and more. Recent studies demonstrate significant homologies between Borrelia components and thyroid system or cardiac muscle host tissues at the molecular level.

Thus an auto-immune attack may occur by mistake and contribute to disease pathology or even be a mechanism adapted by parasites to downregulate needed host defenses. In general these studies do not address the persistence of Borrelia as a persistent stimulus to host autoimmune dysfunctions.

Clinicians treating chronic Lyme with chronic antibiotics often find that initial autoimmune markers found associated with Lyme Disease patients decrease in titer and then disappear along with the clinical evidence of persistent illness. This is found, for example, in positive ANA titers, positive Rheumatoid factor levels, positive anti thyroglobulin levels, positive anti cardiolipin levels etc.

This is so common that if a battery inclusive of a wide range of "auto antibodies" were done on every chronic Lyme Disease patient, then a heterogeneous but everpresent display of molecular mimicry would be expected. The decrease and then disappearance of these markers with antibiotic treatment is evidence that the continued immune dysfunction of self attack is dependent not only on continued near homologies with the germs but also with the continued presence of the microbes- even though the germ load at later stages of treatment may be more at a smoldering infection of little fires in niche tissue sites ie similar to persistent vaccination.

Our immune system has evolved so advanced in recognizing self from dangers of pathogens that it may not be likely that the switch is turned on so absolutely by pathogen mimicry that is not absolute. Can patented pharmaceuticals be so discrete as to target the immune mimicry switches without impairing essential other host immune messages and messengers? Or would it be better to follow the path of microbe eradication and downregulation of host immune dysfunction as a natural course?