Premium
Possible Involvement of IL‐12 in Reovirus Type‐2‐Induced Diabetes in Newborn DBA/1 Mice
Author(s) -
Hayashi T.,
Morimoto M.,
Iwata H.,
Onodera T.
Publication year - 2001
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1046/j.1365-3083.2001.00907.x
Subject(s) - insulitis , spleen , immunology , messenger rna , immune system , monoclonal antibody , biology , cytokine , interleukin 4 , interferon , antibody , autoimmunity , gene , biochemistry
This study extends our previous observations that the reovirus type‐2(Reo‐2) can induce autoimmune insulitis, which may be mediated by T‐helper(Th)1‐dependent mechanisms, resulting in diabetes in newborn DBA/1 mice. In this study mRNA expression for Th1‐related cytokines including Th1 and Th2 cytokines in splenic cells was examined by reverse transcriptase polymerase chain reaction (RT–PCR) in relation to the development of insulitis. Furthermore, the effect of monoclonal antibody (MoAb) against interleukin (IL)‐12(p40) on the development of insulitis and the mRNA expression in the splenic cells was examined. The mRNA expression for IL‐12(p40), IL‐18, and interferon (IFN)‐γ, but not IL‐5, increased in the spleen in parallel with the development of insulitis. The treatment with MoAb to IL‐12(p40) reduced the insulitis with diabetes which was associated with a decrease in the mRNA expression for IL‐12(p40), IL‐18 and IFN‐γ, and an increase of IL‐4 mRNA expression in the spleen. The present study suggested that Th1‐dominant systemic immune responses, being responsible for the development of autoimmune insulitis, might be induced by IL‐12‐induced and IL‐18‐activated mechanisms.