pubmed-article:1675629 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:1675629 | lifeskim:mentions | umls-concept:C0006840 | lld:lifeskim |
pubmed-article:1675629 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
pubmed-article:1675629 | lifeskim:mentions | umls-concept:C0026724 | lld:lifeskim |
pubmed-article:1675629 | lifeskim:mentions | umls-concept:C0024264 | lld:lifeskim |
pubmed-article:1675629 | lifeskim:mentions | umls-concept:C1332714 | lld:lifeskim |
pubmed-article:1675629 | lifeskim:mentions | umls-concept:C0683598 | lld:lifeskim |
pubmed-article:1675629 | pubmed:issue | 7 | lld:pubmed |
pubmed-article:1675629 | pubmed:dateCreated | 1991-7-24 | lld:pubmed |
pubmed-article:1675629 | pubmed:abstractText | The role of CD4+ lymphocytes in resistance of N:NIH(S) III bg/bg nu/+ mice to mucosal candidiasis was evaluated. Alimentary tract colonization with a pure culture of Candida albicans induced a population of lymphocytes in both the Peyer's patches and spleens of bg/bg nu/+ mice, but not bg/bg nu/nu mice, that proliferated and produced interleukin-2 (IL-2) in response to C. albicans antigens. The induction of candida-specific lymphocytes correlated with the clearance of C. albicans from the esophagus and tongue of resistant bg/bg nu/+ mice. Isogenic bg/bg nu/nu mice which do not develop candida-reactive lymphocytes were unable to clear C. albicans from their tongues and esophagi. Treatment of bg/bg nu/+ mice with anti-CD4+ monoclonal antibodies depleted their CD4+ lymphocytes and increased their susceptibility to mucosal candidiasis of the tongue and esophagus. In vivo treatment of bg/bg nu/+ mice with anti-IL-2, anti-gamma interferon (IFN-gamma), or both anti-IL-2 and anti-IFN-gamma monoclonal antibodies did not abrogate their resistance to mucosal candidiasis. Furthermore, treatment of C. albicans-susceptible bg/bg nu/nu mice with IFN-gamma and IL-2 did not protect them from mucosal candidiasis. Thus, CD4+ cells apparently play a critical role in resistance to mucosal candidiasis; however, we were unable to demonstrate a role for IL-2 and IFN-gamma in mediating resistance to mucosal candidiasis. | lld:pubmed |
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pubmed-article:1675629 | pubmed:language | eng | lld:pubmed |
pubmed-article:1675629 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1675629 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:1675629 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:1675629 | pubmed:month | Jul | lld:pubmed |
pubmed-article:1675629 | pubmed:issn | 0019-9567 | lld:pubmed |
pubmed-article:1675629 | pubmed:author | pubmed-author:BalishEE | lld:pubmed |
pubmed-article:1675629 | pubmed:author | pubmed-author:CantornaM TMT | lld:pubmed |
pubmed-article:1675629 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:1675629 | pubmed:volume | 59 | lld:pubmed |
pubmed-article:1675629 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:1675629 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:1675629 | pubmed:pagination | 2447-55 | lld:pubmed |
pubmed-article:1675629 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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pubmed-article:1675629 | pubmed:year | 1991 | lld:pubmed |
pubmed-article:1675629 | pubmed:articleTitle | Role of CD4+ lymphocytes in resistance to mucosal candidiasis. | lld:pubmed |
pubmed-article:1675629 | pubmed:affiliation | Department of Surgery, University of Wisconsin Medical School, Madison 53706. | lld:pubmed |
pubmed-article:1675629 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:1675629 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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