| Autor: |
Henning G; Institute for Clinical and Molecular Virology, University Erlangen-Nürnberg, Erlangen, Germany., Kraft MS, Derfuss T, Pirzer R, de Saint-Basile G, Aversa G, Fleckenstein B, Meinl E |
| Jazyk: |
angličtina |
| Zdroj: |
European journal of immunology [Eur J Immunol] 2001 Sep; Vol. 31 (9), pp. 2741-50. |
| DOI: |
10.1002/1521-4141(200109)31:9<2741::aid-immu2741>3.0.co;2-6 |
| Abstrakt: |
Signaling lymphocytic activation molecule (SLAM) is a CD2-related surface receptor expressed by activated T cells and B cells. SLAM is a self ligand and enhances T cellular proliferation and IFN-gamma production. A defective SLAM associated protein (SAP) causes X-linked lymphoproliferative syndrome (XLP), a frequently lethal mononucleosis based on the inability to control EBV. We report that SLAM augments TCR-mediated cytotoxicity. In normal CD4(+) and CD8(+) T cells, SLAM enhanced TCR-mediated cytotoxicity. In CD4(+) and CD8(+) Herpesvirus saimiri (H.saimiri) infected T cells, SLAM engagement alone triggered cytotoxicity. Using H.saimiri-transformed T cells as a model system we found that SLAM-engagement promotes the release of lytic granules and a CD95-independent killing that requires extracellular Ca(2+), cytoskeletal rearrangements, and signaling mediated by mitogen-activated protein kinase kinases MEK1/2. SLAM-enhanced cytotoxicity implies an immunoregulatory function by facilitating the elimination of APC and a role in overcoming infections with pathogens requiring a cytotoxic immune response. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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