T helper cell subsets in insulin-dependent diabetes.
It has been proposed that the development of insulin-dependent diabetes is controlled by the T helper 1 (TH1) versus TH2 phenotype of autoreactive TH cells: TH1 cells would promote diabetes, whereas TH2 cells would actually protect from disease. This proposition was tested by establishing cultures of TH1 and TH2 cells that express an identical diabetogenic T cell receptor and comparing their ability to initiate disease in neonatal nonobese diabetic mice. TH1-like cells actively promoted diabetes; TH2-like cells invaded the islets but did not provoke disease--neither did they provide substantial protection.
Katz
J D
JD
Institut de Génétique et de Biologie Moléculaire et Cellulaire, INSERM-CNRS-Université Louis Pasteur, Illkirch, CU de Strasbourg, France.
Benoist
C
C
Mathis
D
D
D000818:Animals; D000831:Animals, Newborn; D015551:Autoimmunity / Q000276:immunology; D002465:Cell Movement / Q000276:immunology; D002478:Cells, Cultured; D003922:Diabetes Mellitus, Type 1 / Q000276:immunology*; D007515:Islets of Langerhans / Q000276:immunology; D008213:Lymphocyte Activation / Q000276:immunology; D051379:Mice; D016688:Mice, Inbred NOD; D008822:Mice, Transgenic; D016693:Receptors, Antigen, T-Cell, alpha-beta / Q000235:genetics / Q000276:immunology; D013154:Spleen / Q000166:cytology; D018417:Th1 Cells / Q000276:immunology* / Q000637:transplantation; D018418:Th2 Cells / Q000276:immunology* / Q000637:transplantation
D016693:Receptors, Antigen, T-Cell, alpha-beta