Matches in SemOpenAlex for { <https://semopenalex.org/work/W4313376939> ?p ?o ?g. }
- W4313376939 endingPage "5867" @default.
- W4313376939 startingPage "5860" @default.
- W4313376939 abstract "Abstract The regulation of apoptosis in mature CD4+ or CD8+ αβ+ T cells has been well studied. How the survival and death is regulated in peripheral CD4−CD8− (double negative, DN) αβ+ T cells remains unknown. Recent studies suggest that peripheral DN T cells may play an important role in the regulation of the immune responses mediated by CD4+ or CD8+ T cells. Here, we used immunosuppressive DN T cell clones to elucidate the mechanisms involved in the regulation of death and survival of αβ+ DN T cells. The DN T cell clones were generated from the spleen cells of 2C transgenic mice, which express the transgenic TCR specific for Ld and permanently accepted Ld+ skin allografts after pretransplant infusion of Ld+ lymphocytes. We report that 1) the mature DN T cells are highly resistant to TCR cross-linking-induced apoptosis in the presence of exogenous IL-4; 2) Fas/Fas-ligand and TNF-α/TNFR pathways do not play an apparent role in regulating apoptosis in DN T cells; 3) the DN T cells constitutively express a high level of Bcl-xL, but not Bcl-2; 4) both Bcl-xL and Bcl-2 are up-regulated following TCR-cross-linking; and 5) IL-4 stimulation significantly up-regulates Bcl-xL and c-Jun expression and leads to mitogen-activated protein kinase phosphorylation in DN T cells, which may contribute to the resistance to apoptosis in these T cells. Taken together, these results provide us with an insight into how mature DN T cells resist activation-induced apoptosis to provide a long-term suppressor function in vivo." @default.
- W4313376939 created "2023-01-06" @default.
- W4313376939 creator A5030865232 @default.
- W4313376939 creator A5059310975 @default.
- W4313376939 creator A5065806351 @default.
- W4313376939 creator A5066716873 @default.
- W4313376939 creator A5079495961 @default.
- W4313376939 creator A5086705699 @default.
- W4313376939 date "1999-05-15" @default.
- W4313376939 modified "2023-10-06" @default.
- W4313376939 title "Regulation of Apoptosis in Mature αβ+CD4−CD8− Antigen-Specific Suppressor T Cell Clones" @default.
- W4313376939 cites W1516581843 @default.
- W4313376939 cites W1537606049 @default.
- W4313376939 cites W1566367955 @default.
- W4313376939 cites W1572448432 @default.
- W4313376939 cites W1584666781 @default.
- W4313376939 cites W1592901497 @default.
- W4313376939 cites W1594989289 @default.
- W4313376939 cites W1644097450 @default.
- W4313376939 cites W1821146811 @default.
- W4313376939 cites W1945355049 @default.
- W4313376939 cites W1959540802 @default.
- W4313376939 cites W1975356481 @default.
- W4313376939 cites W1976385326 @default.
- W4313376939 cites W1977133647 @default.
- W4313376939 cites W1979971440 @default.
- W4313376939 cites W1982332591 @default.
- W4313376939 cites W1984866351 @default.
- W4313376939 cites W1987931310 @default.
- W4313376939 cites W1992850639 @default.
- W4313376939 cites W1995465918 @default.
- W4313376939 cites W1996350333 @default.
- W4313376939 cites W1997954665 @default.
- W4313376939 cites W2004645606 @default.
- W4313376939 cites W2008987764 @default.
- W4313376939 cites W2019329111 @default.
- W4313376939 cites W2023809975 @default.
- W4313376939 cites W2025447211 @default.
- W4313376939 cites W2028111124 @default.
- W4313376939 cites W2031418665 @default.
- W4313376939 cites W2033801757 @default.
- W4313376939 cites W2035147500 @default.
- W4313376939 cites W2043395027 @default.
- W4313376939 cites W2045380568 @default.
- W4313376939 cites W2045843248 @default.
- W4313376939 cites W2047777032 @default.
- W4313376939 cites W2057257609 @default.
- W4313376939 cites W2060474886 @default.
- W4313376939 cites W2063176993 @default.
- W4313376939 cites W2065413461 @default.
- W4313376939 cites W2074820885 @default.
- W4313376939 cites W2076779192 @default.
- W4313376939 cites W2080824974 @default.
- W4313376939 cites W2085270426 @default.
- W4313376939 cites W2086313080 @default.
- W4313376939 cites W2091783976 @default.
- W4313376939 cites W2092377971 @default.
- W4313376939 cites W2096613892 @default.
- W4313376939 cites W2099000660 @default.
- W4313376939 cites W2107307935 @default.
- W4313376939 cites W2109372137 @default.
- W4313376939 cites W2112650043 @default.
- W4313376939 cites W2123642439 @default.
- W4313376939 cites W2131616553 @default.
- W4313376939 cites W2134372981 @default.
- W4313376939 cites W2152213870 @default.
- W4313376939 cites W2159162888 @default.
- W4313376939 cites W2171240745 @default.
- W4313376939 cites W2258639618 @default.
- W4313376939 cites W2408046396 @default.
- W4313376939 cites W2439164895 @default.
- W4313376939 doi "https://doi.org/10.4049/jimmunol.162.10.5860" @default.
- W4313376939 hasPublicationYear "1999" @default.
- W4313376939 type Work @default.
- W4313376939 citedByCount "14" @default.
- W4313376939 countsByYear W43133769392012 @default.
- W4313376939 countsByYear W43133769392013 @default.
- W4313376939 countsByYear W43133769392022 @default.
- W4313376939 crossrefType "journal-article" @default.
- W4313376939 hasAuthorship W4313376939A5030865232 @default.
- W4313376939 hasAuthorship W4313376939A5059310975 @default.
- W4313376939 hasAuthorship W4313376939A5065806351 @default.
- W4313376939 hasAuthorship W4313376939A5066716873 @default.
- W4313376939 hasAuthorship W4313376939A5079495961 @default.
- W4313376939 hasAuthorship W4313376939A5086705699 @default.
- W4313376939 hasBestOaLocation W43133769391 @default.
- W4313376939 hasConcept C120642132 @default.
- W4313376939 hasConcept C129374314 @default.
- W4313376939 hasConcept C153911025 @default.
- W4313376939 hasConcept C154317977 @default.
- W4313376939 hasConcept C167672396 @default.
- W4313376939 hasConcept C190283241 @default.
- W4313376939 hasConcept C19317047 @default.
- W4313376939 hasConcept C202751555 @default.
- W4313376939 hasConcept C203014093 @default.
- W4313376939 hasConcept C2776090121 @default.
- W4313376939 hasConcept C31573885 @default.
- W4313376939 hasConcept C55493867 @default.