000114724 001__ 114724
000114724 005__ 20180317092010.0
000114724 0247_ $$2doi$$a10.1073/pnas.94.25.13844
000114724 037__ $$aARTICLE
000114724 245__ $$aInterferon-gamma impacts at multiple points during the progression of autoimmune diabetes
000114724 269__ $$a1997
000114724 260__ $$c1997
000114724 336__ $$aJournal Articles
000114724 500__ $$aUniv Strasbourg 1,Cnrs,Inserm,Inst Genet & Biol Mol & Cellulaire,F-67404 Illkirch Graffens,France Ludwig Inst Canc Res,Ch-1066 Epalinges,Switzerland
000114724 520__ $$aThe role of interferon-gamma in autoimmune diabetes was assessed by breeding a null mutation of the interferon-gamma receptor of chain into the nonobese diabetic mouse strain, as well as into a simplified T cell receptor transgenic model of diabetes. In contrast to a previous report on abrogation of the interferon-gamma gene, mutation of the gene encoding its receptor led to drastic effects on disease in both mouse lines. Nonobese diabetic mice showed a marked inhibition of insulitis-both the kinetics and penetrance-and no signs of diabetes; the transgenic model exhibited near-normal insulitis, but this never evolved into diabetes, either spontaneously or after experimental provocation. This failure could not be explained by perturbations in the ratio of T helper cell phenotypes; rather, it reflected a defect in antigen-presenting cells or in the islet beta cell targets.
000114724 700__ $$aWang, B.
000114724 700__ $$aAndre, I.
000114724 700__ $$aGonzalez, A.
000114724 700__ $$aKatz, J. D.
000114724 700__ $$0240585$$aAguet, M.$$g168669
000114724 700__ $$aBenoist, C.
000114724 700__ $$aMathis, D.
000114724 773__ $$j94$$k25$$q13844-13849$$tProceedings of the National Academy of Sciences of the United States of America
000114724 909CO $$ooai:infoscience.tind.io:114724$$particle$$pSV
000114724 909C0 $$0252150$$pUPAGU$$xU11156
000114724 937__ $$aUPAGU-ARTICLE-1997-004
000114724 973__ $$aOTHER$$rREVIEWED$$sPUBLISHED
000114724 980__ $$aARTICLE