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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
10
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pubmed:dateCreated |
1990-10-24
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pubmed:abstractText |
The ability of antigen-specific T-helper (Th) cells to enhance direct plaque-forming cell responses in spleen cells from Trypanosoma cruzi-infected C57BL/6 mice was investigated at various times during the course of infection from day 7 to day 230. The injection of antigen-specific Th cells in vivo or the addition of antigen-specific Th cells in vitro was effective in enhancing direct plaque-forming cell responses, except at the time of the most intense suppression during the acute phase of infection (i.e., day 28). The ability of antigen-specific Th cells to overcome nonspecific immunosuppression was due not only to the activity of antigen-specific Th cells added to Mishel-Dutton cultures but also to activation of resident T cells. Thus, antigen-specific Th cells and resident T cells act in concert to produce enhanced direct plaque-forming cell responses. The effect of plastic-adherent spleen cells from infected mice on the ability of antigen-specific Th cells to stimulate anti-sheep erythrocyte responses of normal spleen cells was examined because macrophages have been shown to have an immunoregulatory role during the course of experimental American trypanosomiasis. Increasing numbers of macrophages from infected mice caused increased immunosuppression of normal spleen cells that could not be overcome with the addition of primed Th cells. It can be concluded from these data that antigen-specific Th cells can potentiate immune responses in mice infected with T. cruzi but that highly active suppressor macrophages can inhibit the expression of these primed Th cells.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/1698177-210036,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1698177-2965730,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1698177-3932205,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1698177-402286,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1698177-4587740,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1698177-4615402,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1698177-6218465,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1698177-6225801,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1698177-6235290,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1698177-6407015,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1698177-6411359,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1698177-6431001,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1698177-6767829,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1698177-6811661
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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 |
Oct
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pubmed:issn |
0019-9567
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
58
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
3248-56
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:1698177-Analysis of Variance,
pubmed-meshheading:1698177-Animals,
pubmed-meshheading:1698177-Cells, Cultured,
pubmed-meshheading:1698177-Chagas Disease,
pubmed-meshheading:1698177-Epitopes,
pubmed-meshheading:1698177-Erythrocytes,
pubmed-meshheading:1698177-Female,
pubmed-meshheading:1698177-Hemolytic Plaque Technique,
pubmed-meshheading:1698177-Immune Tolerance,
pubmed-meshheading:1698177-Macrophages,
pubmed-meshheading:1698177-Mice,
pubmed-meshheading:1698177-Mice, Inbred C57BL,
pubmed-meshheading:1698177-Spleen,
pubmed-meshheading:1698177-T-Lymphocytes, Helper-Inducer,
pubmed-meshheading:1698177-Trypanosoma cruzi
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pubmed:year |
1990
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pubmed:articleTitle |
Antigen-specific T-helper cells abrogate suppression in Trypanosoma cruzi-infected mice.
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pubmed:affiliation |
Department of Biology, Wake Forest University, Winston-Salem, North Carolina 27109.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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