Suppression of cyclophosphamide induced diabetes development and pancreatic Th1 reactivity in NOD mice treated with the interleukin (IL)-12 antagonist IL-12[p40)2

Diabetologia

Volumn 40, Issue 6, 1997, Pages 641-646

  Rothe, H ^a,c   O'Hara Jr , R M ^b   Martin, S ^a   Kolb, H ^a  

^a HEINRICH HEINE UNIVERSITY   (Germany)

^b PFIZER INC   (United States)

^c LEIBNIZ CENTER FOR DIABETES RESEARCH AT HEINRICH HEINE UNIVERSITY DÜSSELDORF   (Germany)

Author keywords

IL 12 antagonist; Inducible NO synthase; Insulitis; NOD mouse; Th1 Th2 balance

Indexed keywords

CYCLOPHOSPHAMIDE; GAMMA INTERFERON; INTERLEUKIN 12; NITRIC OXIDE SYNTHASE;

ANIMAL EXPERIMENT; ANIMAL TISSUE; ARTICLE; AUTOIMMUNITY; DIABETES MELLITUS; IMMUNE RESPONSE; INSULITIS; MACROPHAGE; MOUSE; NONHUMAN; PATHOGENESIS; PRIORITY JOURNAL;

ANIMALS; CYCLOPHOSPHAMIDE; DIABETES MELLITUS, TYPE 1; DIMERIZATION; FEMALE; INTERFERON TYPE II; INTERLEUKIN-10; INTERLEUKIN-12; ISLETS OF LANGERHANS; MACROPHAGES, PERITONEAL; MICE; MICE, INBRED NOD; NITRIC OXIDE SYNTHASE; PANCREAS; RNA, MESSENGER; TH1 CELLS; TRANSCRIPTION, GENETIC; TUMOR NECROSIS FACTOR-ALPHA;

EID: 0030789325     PISSN: 0012186X     EISSN: None     Source Type: Journal    
DOI: 10.1007/s001250050728     Document Type: Article

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