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Mechanisms of V1 T Cell Activation by Microbial Components¹

Hiranmoy Das^*, Masahiko Sugita and Michael B. Brenner^2,*

^* Division of Rheumatology, Immunology, and Allergy, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA 02115; and Department of Microbiology and Immunology, Nippon Medical School, Tokyo, Japan

There are two major subsets of T cell in humans. V2V2 T cells predominate in the circulation and significantly expand in vivo during a variety of infectious diseases. Ags identified for the V2 T cells are nonpeptide phosphate, amine, and aminobisphosphonate compounds. In contrast, V1-encoded TCRs account for the vast majority of T cells in tissues such as intestine and spleen. Some of these T cells recognize CD1c and MHC class I-related chain B molecules. These T cells are cytotoxic and use both perforin- and Fas-mediated cytotoxicity. A fundamental question is how these T cells are activated during microbial exposure to carry out effector functions. In this study, we provide evidence for a mechanism by which V1 T cells are activated by inflammatory cytokines in the context of the V1 TCR. Dendritic cells are necessary as accessory cells for microbial Ag-mediated V1 T cell activation. Cytokine (IL-12), adhesion (LFA3/CD2, LFA1/ICAM1) and costimulatory (MHC class I-related chain B molecule/NK-activating receptor G2D) molecules play a significant role along with V1 TCR in this activation.

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