Immunomodulation of the anti-islet CD8 T cell response by B7-2

Deepak Yadav, Nora Sarvetnick

Research output: Contribution to journalArticle

3 Citations (Scopus)

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 languageEnglish (US)
Pages (from-to)221-226
Number of pages6
JournalJournal of Clinical Immunology
Volume27
Issue number2
DOIs
StatePublished - Mar 1 2007

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Immunomodulation
T-Lymphocytes
Inbred NOD Mouse
Autoimmunity
Adoptive Transfer
Cell Survival
Lymph Nodes

Keywords

  • B7-2
  • CD8 T cell
  • Costimulation
  • Type 1 diabetes

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

Cite this

Immunomodulation of the anti-islet CD8 T cell response by B7-2. / Yadav, Deepak; Sarvetnick, Nora.

In: Journal of Clinical Immunology, Vol. 27, No. 2, 01.03.2007, p. 221-226.

Research output: Contribution to journalArticle

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