Open AccessInduction of autoimmune disease by graft‐ versus host reaction across MHC class II difference: modification of the lesions in IL‐6 transgenic mice
Author(s) -
KIMURA T.,
SUZUKI K.,
INADA S.,
HAYASHI A.,
SAITO H.,
MIYAI T.,
MATSUZAKI Y.,
TANAKA N.,
OSDGA T.,
FUJIWARA M.
Publication year - 1994
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.1994.tb07030.x
Subject(s) - immunology , spleen , primary biliary cirrhosis , genetically modified mouse , mhc class ii , autoimmune disease , transgene , biology , major histocompatibility complex , antibody , antigen , genetics , gene
SUMMARY 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)F 1 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.