TY - JOUR
T1 - IL-10 is necessary and sufficient for autoimmune diabetes in conjunction with NOD MHC homozygosity
AU - Lee, Myung Shik
AU - Mueller, Regula
AU - Wicker, Linda S.
AU - Peterson, Laurence B.
AU - Sarvetnick, Nora
PY - 1996/6/1
Y1 - 1996/6/1
N2 - Contrary to expectations based on in vitro experiments, we previously found that pancreatic IL-10 did not inhibit autoimmune diabetes but accelerated it in an MHC-dependent manner. Therefore, the ability of IL-10 to overcome the absence of all non-MHC diabetes susceptibility (Idd) alleles was studied in transgenic mice expressing pancreatic IL-10 backcrossed to B10.H2(g7) congenic mice, which have no Idd alleles other than NOD MHC (H2(g7)). IL-10 transgenic backcross 1 (BC1) mice with H2(g7/g7) haplotype developed clear-cut insulitis and diabetes, but neither transgenic mice with the H2(g/b) haplotype nor nontransgenic BCL mice did so. Further implicating IL-10 in autoimmune diabetes, anti-IL-10 antibody treatment inhibited the development of insulitis in NOD mice. These results suggest that IL-10 may be necessary and sufficient for producing autoimmune diabetes in conjunction with NOD MHC homozygosity and that some Idd genes may be related to the regulation of IL-10.
AB - Contrary to expectations based on in vitro experiments, we previously found that pancreatic IL-10 did not inhibit autoimmune diabetes but accelerated it in an MHC-dependent manner. Therefore, the ability of IL-10 to overcome the absence of all non-MHC diabetes susceptibility (Idd) alleles was studied in transgenic mice expressing pancreatic IL-10 backcrossed to B10.H2(g7) congenic mice, which have no Idd alleles other than NOD MHC (H2(g7)). IL-10 transgenic backcross 1 (BC1) mice with H2(g7/g7) haplotype developed clear-cut insulitis and diabetes, but neither transgenic mice with the H2(g/b) haplotype nor nontransgenic BCL mice did so. Further implicating IL-10 in autoimmune diabetes, anti-IL-10 antibody treatment inhibited the development of insulitis in NOD mice. These results suggest that IL-10 may be necessary and sufficient for producing autoimmune diabetes in conjunction with NOD MHC homozygosity and that some Idd genes may be related to the regulation of IL-10.
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U2 - 10.1084/jem.183.6.2663
DO - 10.1084/jem.183.6.2663
M3 - Article
C2 - 8676087
AN - SCOPUS:0029896602
VL - 183
SP - 2663
EP - 2668
JO - Journal of Experimental Medicine
JF - Journal of Experimental Medicine
SN - 0022-1007
IS - 6
ER -