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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
11
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pubmed:dateCreated |
1990-6-28
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pubmed:abstractText |
In addition to previous evidence for the roles of T cell-dependent immunity and delayed-type hypersensitivity in acquired resistance to systemic candidosis in mice, in the present study we have investigated the relative contributions of L3T4+ and Lyt-2+ lymphocytes in the protective immunity induced by vaccination with low virulence Candida albicans cells. We have also addressed the issue of the mode of Candida Ag recognition by specific T cells leading to cytokine release. Spleen cells from immunized mice produced high levels of IFN-gamma in vitro in response to Candida Ag, and this activity was abolished only by the combined treatment of the responder population with anti-L3T4 and anti-Lyt-2.2 mAb plus C. Positively selected L3T4+ and Lyt-2+ cells also produced IFN-gamma in vitro, provided accessory cells (plastic-adherent and Thy-1- Ia- splenocytes, respectively) were added to the lymphocyte-yeast cell cocultures. The production of IFN-gamma by purified L3T4+ and Lyt-2+ cells was inhibited by addition of the respective anti-class II and anti-class I H-2 antibody to the cultures. In vivo, administration of anti-L3T4, anti-Lyt-2.2 mAb or a combination of both significantly impaired the resistance of immunized mice to challenge with virulent C. albicans, as manifested by increased recovery of the yeast from the mouse kidneys. A similar effect was observed upon neutralization of endogenous IFN-gamma by treatment with rat mAb. These results suggest that both L3T4+ and Lyt-2+ T cells play a role in acquired immunity to systemic C. albicans infection, and that their activity may involve IFN-gamma-mediated stimulation of candidacidal mechanisms.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antibodies, Monoclonal,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Ly,
http://linkedlifedata.com/resource/pubmed/chemical/H-2 Antigens,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon-gamma,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-2
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
0022-1767
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
144
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
4333-9
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:1971296-Animals,
pubmed-meshheading:1971296-Antibodies, Monoclonal,
pubmed-meshheading:1971296-Antigens, Ly,
pubmed-meshheading:1971296-CD4-Positive T-Lymphocytes,
pubmed-meshheading:1971296-Candidiasis,
pubmed-meshheading:1971296-Female,
pubmed-meshheading:1971296-H-2 Antigens,
pubmed-meshheading:1971296-Hypersensitivity, Delayed,
pubmed-meshheading:1971296-Immunity, Cellular,
pubmed-meshheading:1971296-Immunization,
pubmed-meshheading:1971296-Interferon-gamma,
pubmed-meshheading:1971296-Interleukin-2,
pubmed-meshheading:1971296-Kidney,
pubmed-meshheading:1971296-Lymphocyte Activation,
pubmed-meshheading:1971296-Mice,
pubmed-meshheading:1971296-T-Lymphocytes
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pubmed:year |
1990
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pubmed:articleTitle |
T cell subsets and IFN-gamma production in resistance to systemic candidosis in immunized mice.
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pubmed:affiliation |
Department of Experimental Medicine and Biochemical Sciences, University of Perugia, Italy.
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pubmed:publicationType |
Journal Article,
In Vitro
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