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  • 1
    Publication Date: 1995-04-21
    Description: Bacterial superantigens bind with high affinity to major histocompatibility complex (MHC) class II antigens on antigen-presenting cells and with T cell antigen receptor (TCR) beta chains on T lymphocytes, which results in the T cell activation responsible for toxic shock syndrome and food poisoning. Many cytotoxic T lymphocyte (CTL) clones were shown to have receptors for human leukocyte antigen (HLA) class I molecules that inhibited superantigen-induced cytotoxicity against appropriate class I-bearing target cells. One type of inhibitory receptor, NKB1, was present on CD4+ and CD8+TCR alpha beta+ CTL clones and blocked the killing of staphylococcal enterotoxin B (SEB)-coated targets bearing certain polymorphic HLA-B molecules. Expression of HLA-A, -B, and -C molecules on the SEB-coated targets also protected against cytolysis mediated by many NKB1-negative T cell clones, suggesting the presence of additional inhibitory MHC class I receptors. These HLA class I receptors may limit tissue destruction and possibly autoimmunity caused by activated T lymphocytes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Phillips, J H -- Gumperz, J E -- Parham, P -- Lanier, L L -- AI22039/AI/NIAID NIH HHS/ -- GM07276/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1995 Apr 21;268(5209):403-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Human Immunology, DNAX Research Institute of Molecular and Cellular Biology, Palo Alto, CA 94304, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7716542" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; *Cytotoxicity, Immunologic ; Enterotoxins/immunology ; HLA-A Antigens/immunology ; HLA-B Antigens/immunology ; HLA-C Antigens/immunology ; Humans ; Receptors, Antigen, T-Cell/*immunology ; Receptors, Antigen, T-Cell, alpha-beta/immunology ; Receptors, Immunologic/*immunology ; Receptors, KIR ; Receptors, KIR3DL1 ; Superantigens/*immunology ; T-Lymphocytes, Cytotoxic/*immunology ; Transfection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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