IL-10 deficiency does not inhibit insulitis and accelerates cyclophosphamide-induced diabetes in the nonobese diabetic mouse.
IL-10 exterts profound immunostimulatory and immunoinhibitory effects. To explore the role of IL-10 in autoimmune diabetes of nonobese diabetic (NOD) mice, we generated IL-10-deficient NOD mice. In contrast to our previous results with neutralizing antibodies to IL-10, IL-10-deficient NOD mice developed insulitis and their splenocytes readily responded to islet antigen glutamic acid decarboxylase 65. IL-10-deficient NOD mice did not develop accelerated spontaneous diabetes. On the other hand, IL-10-deficient NOD mice developed accelerated disease following cyclophosphamide (CYP) injection. These findings demonstrate that IL-10 is dispensable for autoimmune diabetes. IL-10's absence fails to accelerate endogenous diabetes but potentiates CYP-induced diabetes.
Balasa
B
B
Department of Immunology, The Scripps Research Institute, La Jolla, California 92037, USA.
Van Gunst
K
K
Jung
N
N
Katz
J D
JD
Sarvetnick
N
N
D000818:Animals; D000941:Antigens / Q000276:immunology; D003520:Cyclophosphamide / Q000494:pharmacology; D003922:Diabetes Mellitus, Type 1 / Q000139:chemically induced / Q000276:immunology* / Q000473:pathology; D005968:Glutamate Decarboxylase / Q000276:immunology; D016753:Interleukin-10 / Q000172:deficiency / Q000235:genetics / Q000502:physiology*; D007515:Islets of Langerhans / Q000276:immunology; D007527:Isoenzymes / Q000276:immunology; D051379:Mice; D008810:Mice, Inbred C57BL; D016688:Mice, Inbred NOD; D018345:Mice, Knockout; D010195:Pancreatitis / Q000276:immunology* / Q000473:pathology; D013601:T-Lymphocytes / Q000276:immunology
D000941:Antigens; D007527:Isoenzymes; D016753:Interleukin-10; D003520:Cyclophosphamide; D005968:Glutamate Decarboxylase; C401141:glutamate decarboxylase 2