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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
5
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pubmed:dateCreated |
2001-3-6
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pubmed:abstractText |
Similarities in the phenotypes of mice deficient for cytotoxic T lymphocyte antigen-4 (CTLA-4) or transforming growth factor-beta1 (TGF-beta1) and other observations have led to speculation that CTLA-4 mediates its inhibitory effect on T cell activation via costimulation of TGF-beta production. Here, we examine the role of TGF-beta in CTLA-4-mediated inhibition of T cell activation and of CTLA-4 in the regulation of TGF-beta production. Activation of AND TCR transgenic mouse T cells with costimulatory receptor-specific antigen presenting cells results in efficient costimulation of proliferation by CD28 ligation and inhibition by CTLA-4 ligation. Neutralizing antibody to TGF-beta does not reverse CTLA-4-mediated inhibition. Also, CTLA-4 ligation equally inhibits proliferation of wild-type, TGF-beta1(-/-), and Smad3(-/-) T cells. Further, CTLA-4 engagement does not result in the increased production of either latent or active TGF-beta by CD4(+) T cells. These results indicate that CTLA-4 ligation does not regulate TGF-beta production and that CTLA-4-mediated inhibition can occur independently of TGF-beta. Collectively, these data demonstrate that CTLA-4 and TGF-beta represent distinct mechanisms for regulation of T cell responses.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/11226283-10064594,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11226283-10229815,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11226283-10415006,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11226283-10648114,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11226283-10657651,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11226283-10679068,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11226283-10714683,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11226283-10748236,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11226283-10779742,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11226283-10878341,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11226283-10899916,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11226283-11244047,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11226283-1436033,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11226283-2384664,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11226283-2571940,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11226283-2871125,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11226283-3131428,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11226283-7481803,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11226283-7584144,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11226283-8421714,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11226283-8717514,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11226283-8903331,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11226283-8929708,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11226283-9120387,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11226283-9200453,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11226283-9256476,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11226283-9362525,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11226283-9430233,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11226283-9551960,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11226283-9597129,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11226283-9712029,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11226283-9724845,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11226283-9815262,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11226283-9856951
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
0027-8424
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
27
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pubmed:volume |
98
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
2587-92
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:11226283-Animals,
pubmed-meshheading:11226283-Antigen-Presenting Cells,
pubmed-meshheading:11226283-Antigens, CD,
pubmed-meshheading:11226283-Antigens, Differentiation,
pubmed-meshheading:11226283-CD4-Positive T-Lymphocytes,
pubmed-meshheading:11226283-CTLA-4 Antigen,
pubmed-meshheading:11226283-Cell Division,
pubmed-meshheading:11226283-Immunoconjugates,
pubmed-meshheading:11226283-Lymphocyte Activation,
pubmed-meshheading:11226283-Mice,
pubmed-meshheading:11226283-Mice, Inbred C57BL,
pubmed-meshheading:11226283-Mice, Transgenic,
pubmed-meshheading:11226283-Neutralization Tests,
pubmed-meshheading:11226283-Transforming Growth Factor beta
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pubmed:year |
2001
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pubmed:articleTitle |
Lack of a role for transforming growth factor-beta in cytotoxic T lymphocyte antigen-4-mediated inhibition of T cell activation.
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pubmed:affiliation |
Howard Hughes Medical Institute, Cancer Research Laboratory, Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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