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Article: Normal responsiveness of CTLA-4-deficient anti-viral cytotoxic T cells
Title | Normal responsiveness of CTLA-4-deficient anti-viral cytotoxic T cells |
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Authors | |
Issue Date | 1998 |
Citation | Journal of Immunology, 1998, v. 160, n. 1, p. 95-100 How to Cite? |
Abstract | CTLA-4 has been proposed to negatively regulate immune responses, and mice deficient for CTLA-4 expression succumb to a lymphoproliferative disorder within a few weeks after birth. This study assessed the responsiveness of CTLA-4-deficient T cells expressing a class I-restricted TCR specific for lymphocytic choriomeningitis virus (LCMV). The kinetics of T cell proliferation were studied in vitro after stimulation of T cells with full and partial T cell agonists. No gross abnormalities in CTLA-4-deficient T cells could be detected. Using adoptive transfer experiments, T cell responses were also measured in vivo after infection with LCMV. Low dose infection with LCMV leads to strong expansion of specific T cells followed by a reduction in T cells that parallels the elimination of Ag. The kinetics of T cell expansion and elimination after low dose LCMV infection were not affected by the absence of CTLA-4. High dose infection of mice with LCMV leads to a transient expansion of T cells followed by T cell exhaustion, where all specific T cells are eliminated. T cell exhaustion also occurred in the absence of CTLA-4. Thus, surprisingly, the absence of CTLA-4 did not interfere with T cell activation, down-regulation of ongoing T cell responses after the elimination of Ag, or the exhaustion of T cell responses in the presence of excessive amounts of Ag. |
Persistent Identifier | http://hdl.handle.net/10722/291446 |
ISSN | 2021 Impact Factor: 5.426 2020 SCImago Journal Rankings: 2.737 |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Bachmann, Martin F. | - |
dc.contributor.author | Waterhouse, Paul | - |
dc.contributor.author | Speiser, Daniel E. | - |
dc.contributor.author | McKall-Faienza, Kim | - |
dc.contributor.author | Mak, Tak W. | - |
dc.contributor.author | Ohashi, Pamela S. | - |
dc.date.accessioned | 2020-11-17T14:54:23Z | - |
dc.date.available | 2020-11-17T14:54:23Z | - |
dc.date.issued | 1998 | - |
dc.identifier.citation | Journal of Immunology, 1998, v. 160, n. 1, p. 95-100 | - |
dc.identifier.issn | 0022-1767 | - |
dc.identifier.uri | http://hdl.handle.net/10722/291446 | - |
dc.description.abstract | CTLA-4 has been proposed to negatively regulate immune responses, and mice deficient for CTLA-4 expression succumb to a lymphoproliferative disorder within a few weeks after birth. This study assessed the responsiveness of CTLA-4-deficient T cells expressing a class I-restricted TCR specific for lymphocytic choriomeningitis virus (LCMV). The kinetics of T cell proliferation were studied in vitro after stimulation of T cells with full and partial T cell agonists. No gross abnormalities in CTLA-4-deficient T cells could be detected. Using adoptive transfer experiments, T cell responses were also measured in vivo after infection with LCMV. Low dose infection with LCMV leads to strong expansion of specific T cells followed by a reduction in T cells that parallels the elimination of Ag. The kinetics of T cell expansion and elimination after low dose LCMV infection were not affected by the absence of CTLA-4. High dose infection of mice with LCMV leads to a transient expansion of T cells followed by T cell exhaustion, where all specific T cells are eliminated. T cell exhaustion also occurred in the absence of CTLA-4. Thus, surprisingly, the absence of CTLA-4 did not interfere with T cell activation, down-regulation of ongoing T cell responses after the elimination of Ag, or the exhaustion of T cell responses in the presence of excessive amounts of Ag. | - |
dc.language | eng | - |
dc.relation.ispartof | Journal of Immunology | - |
dc.title | Normal responsiveness of CTLA-4-deficient anti-viral cytotoxic T cells | - |
dc.type | Article | - |
dc.description.nature | link_to_OA_fulltext | - |
dc.identifier.pmid | 9551960 | - |
dc.identifier.scopus | eid_2-s2.0-0031905627 | - |
dc.identifier.volume | 160 | - |
dc.identifier.issue | 1 | - |
dc.identifier.spage | 95 | - |
dc.identifier.epage | 100 | - |
dc.identifier.isi | WOS:000071915100015 | - |
dc.identifier.issnl | 0022-1767 | - |