Abstract: |
CD8+ T cells require a signal through a costimulatory receptor in addition to TCR engagement to become activated. The role of CD28 in costimulating T cell activation is well established. NKG2D, a receptor found on NK cells, CD8+ αβ-TCR+ T cells, and γδ-TCR+ T cells, has also been implicated in T cell costimulation. In this study we have evaluated the role of NKG2D in costimulating mouse and human naive and effector CD8+ T cells. Unexpectedly, in contrast to CD28, NK62D engagement by ligand or mAb is not sufficient to costimulate naive or effector CD8+ T cell responses in conventional T cell populations. While NKG2D did not costimulate CD8+ T cells on its own, it was able to modify CD28-mediated costimulation of human CD8+ T cells under certain contitions. It is, therefore, likely that NKG2D acts as a costimulatory molecule only ander restricted conditions or requires additional cofactors. |
Keywords: |
signal transduction; human cell; nonhuman; cd8 antigen; lymphocyte proliferation; t lymphocyte; cd8-positive t-lymphocytes; animal cell; mouse; animals; mice; cells, cultured; cell line, tumor; mice, inbred c57bl; mice, transgenic; monoclonal antibody; t lymphocyte receptor beta chain; t lymphocyte receptor gamma chain; lymphocyte activation; antibodies, monoclonal; immune response; receptors, antigen, t-cell; ligand; melanoma, experimental; ligands; natural killer cell; effector cell; immunostimulation; adjuvants, immunologic; protein cross linking; t lymphocyte activation; antigens, cd28; receptors, immunologic; g0 phase; natural killer cell receptor nkg2d; coculture techniques; t lymphocyte receptor alpha chain; t lymphocyte receptor delta chain; cytotoxicity tests, immunologic; cross-linking reagents; interferon type ii; mice, inbred dba
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