Abstract
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.
Original language | English (US) |
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Pages (from-to) | 221-226 |
Number of pages | 6 |
Journal | Journal of Clinical Immunology |
Volume | 27 |
Issue number | 2 |
DOIs | |
State | Published - Mar 2007 |
Externally published | Yes |
Keywords
- B7-2
- CD8 T cell
- Costimulation
- Type 1 diabetes
ASJC Scopus subject areas
- Immunology and Allergy
- Immunology