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  • 2000-2004  (2)
  • 1
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Hybridomas expressing murine γδ T-cell receptors were found to produce cytokines in response to cardiolipin (CL) and structurally related anionic phospholipids. This response required serum at concentrations related to the amount of CL in cultures. The purified serum factor, β2-glycoprotein 1 (β2-GP1) (apolipoprotein H), supported the CL response alone, whereas several other serum proteins and ovalbumin did not. β2-GP1 is known to form complexes with anionic phospholipids, particularly CL, which are often recognized by pathological autoantibodies. We speculate that γδ T cells also recognize such complexes and that the hybridoma response reported here reflects this specificity.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: In the spleens of mice infected intraperitoneally with the bacterium Listeria monocytogenes, both αβ and γδ T cells became rapidly activated, followed by a massive apoptotic death response predominantly within the γδ population. The death response involved two major splenic γδ T-cell subsets and was Fas/Fas ligand (Fas-L)-dependent. Among T cells isolated from the Listeria-infected spleen, Fas-L was almost exclusively expressed in γδ T cells. γδ T cells coexpressed Fas and Fas-L, suggesting activation-induced suicide as a mechanism of their death. In vivo treatment with an antibody specific for CD3ε induced activation, preferential Fas-L expression and apoptosis of γδ T cells, resembling the response pattern in listeriosis, whereas antibodies specific for T-cell receptor-β (TCR-β) or TCR-δ did not, suggesting that the complete response seen in listeriosis requires both γδ TCR engagement and additional stimuli. L. monocytogenes causes early nonspecific, Fas-independent lymphocyte death in heavily infected tissues. In contrast, the death response described here is selective, Fas-dependent and triggered at low local levels of bacteria, suggesting that it is controlled by interactions with other infection-activated host cells, and perhaps part of a regulatory circuit specifically curtailing γδ T cells.
    Type of Medium: Electronic Resource
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