Induction of autoimmune disease by graft-versus host reaction across MHC class II difference: modification of the lesions in IL-6 transgenic mice

We examined the effect of IL-6 on the development of autoimmune diseases (primary biliary cirrhosis. Sjögren's syndrome) employing murine grari-versus-host reaction (GVHR) model with MHC class II disparity. For this purpose, we used IL-6 transgenic(B6.6) mice in which a high level of IL-6 was detected. C57B1/6 (B6) spleen T cells were injected into B6.6 mated with B6.C-H-2^(bml2) mutant mice ((bmi2x B6.6)F^I) and GVHR with MHC class II disparity was induced. The iransgenic hybrid mice with GVHR showed a larger spleen index and contained a higher serum level of IL-6 than those without GVHR. Autoimmune-like lesions in transgenic recipients became weakened compared with those in non-transgenic (bml2 x B6)F₁ recipients. In contrast, levels of antimitochondrial antibodies in (bm 12 x B6.6)FI GVHR group were signiiicantly higher than that of (bml2 X B6)F_I GVHR group. These results indicate that lL-6 excessively produced in vivo might regulate the progression of autotmmune diseases.