Immunomodulation of the anti-islet CD8 T cell response by B7-2.
The absence of diabetes in NOD mice devoid of B7-2 signifies a critical role played by B7-2 in promoting autoimmunity. We asked whether the CD8 T cell compartment is impacted by the absence of B7-2. We found significantly lower expansion of anti-islet CD8 T cells in B7-2KO mice, although their survival and activation states remained unchanged in the pancreatic lymph nodes (PLNs). CD8 T cells from B7-2KO mice exhibited significantly diminished effector function compared to NOD mice. Adoptive transfer experiments using in vitro activated anti-islet CD8 T cells showed that B7-2 does not control the effector phase of the autoreactive CD8 T cell response. Our data indicate that B7-2 promotes pancreatic autoimmunity by controlling CD8 T cell expansion and effector function, but is dispensable for CD8 T cell activation, survival, and the effector phase of anti-islet CD8 T cell response.
Yadav
Deepak
D
Department of Immunology, Scripps Research Institute, 10550 North Torrey Pines Road, Mail Drop IMM-23, La Jolla, California 92037, USA.
Sarvetnick
Nora
N
D019264:Adoptive Transfer; D000818:Animals; D051940:B7-2 Antigen / Q000235:genetics / Q000276:immunology*; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology*; D003922:Diabetes Mellitus, Type 1 / Q000276:immunology*; D005260:Female; D005434:Flow Cytometry; D007515:Islets of Langerhans / Q000276:immunology*; D008213:Lymphocyte Activation / Q000276:immunology*; D051379:Mice; D016688:Mice, Inbred NOD; D008822:Mice, Transgenic
D051940:B7-2 Antigen