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- W1818042852 abstract "The functions of GPI-anchored proteins in T lymphocyte activation have been controversial. This issue was addressed by studying the responses of T lymphocytes from T lymphocyte-specific GPI anchor-deficient mice to different stimuli that normally allow coligation of TCR and GPI-anchored proteins. Stimulation of GPI anchor-deficient T lymphocytes with ConA induced 2-fold higher proliferative responses than did normal cells. In response to allogeneic stimulation, proliferation of GPI anchor-deficient T lymphocytes was enhanced 2- to 3-fold. The response to ConA of a GPI anchor-deficient anti-OVA T lymphocyte clone generated from these mice was approximately 3-fold higher than that of cells from the same clone in which GPI anchor expression was restored by retroviral transduction. The response of the GPI anchor-deficient cloned anti-OVA T lymphocytes to antigenic stimulation was similar to that of the retrovirally restored cells. These results indicate that coligation with GPI-anchored proteins counteracts the response to TCR stimulation by ConA or alloantigen but not protein Ag." @default.
- W1818042852 created "2016-06-24" @default.
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- W1818042852 date "2004-09-15" @default.
- W1818042852 modified "2023-10-11" @default.
- W1818042852 title "Enhanced Responses of Glycosylphosphatidylinositol Anchor-Deficient T Lymphocytes" @default.
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- W1818042852 doi "https://doi.org/10.4049/jimmunol.173.6.3810" @default.
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