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Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555
To provide direct genetic evidence for a role of IL-6 in
experimental autoimmune myasthenia gravis (EAMG), IL-6 gene
KO (IL-6-/-) mice in the C57BL/6 background were
immunized with Torpedo californica acetylcholine receptor
(AChR) and evaluated for EAMG. Only 25% of AChR-immunized
IL-6-/- mice developed clinical EAMG compared to 83% of
C57BL/6 (wild-type) mice. A significant reduction in the secondary
anti-AChR Ab of IgG, IgG2b, and IgG2c, but
not the primary or secondary IgM response was observed in
AChR-immunized IL-6-/- mice, suggesting a possible defect
in T cell help and class switching to anti-AChR IgG2
isotype. The AChR-specific lymphocyte proliferative response, IFN-
,
and IL-10 production were suppressed in AChR-immunized
IL-6-/- mice. EAMG resistance in IL-6-/-
mice was associated with a significant reduction in germinal center
formation and decreased serum complement C3 levels. The data provide
the first direct genetic evidence for a key role of IL-6 in the
autoimmune response to AChR and in EAMG
pathogenesis.
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