| pubmed-article:8450057 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:8450057 | lifeskim:mentions | umls-concept:C0021051 | lld:lifeskim |
| pubmed-article:8450057 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
| pubmed-article:8450057 | lifeskim:mentions | umls-concept:C0237401 | lld:lifeskim |
| pubmed-article:8450057 | lifeskim:mentions | umls-concept:C0021756 | lld:lifeskim |
| pubmed-article:8450057 | lifeskim:mentions | umls-concept:C0231221 | lld:lifeskim |
| pubmed-article:8450057 | lifeskim:mentions | umls-concept:C1819457 | lld:lifeskim |
| pubmed-article:8450057 | lifeskim:mentions | umls-concept:C0392747 | lld:lifeskim |
| pubmed-article:8450057 | lifeskim:mentions | umls-concept:C0443172 | lld:lifeskim |
| pubmed-article:8450057 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:8450057 | pubmed:dateCreated | 1993-4-13 | lld:pubmed |
| pubmed-article:8450057 | pubmed:abstractText | Infection with HIV results in an incremental loss of T helper cell (TH) function, which can occur years before CD4 cell numbers are critically reduced and AIDS is diagnosed. All TH function is not affected, however, because B cell activation and hypergammaglobulinema are also characteristic of this period. Recently, in a murine model of AIDS an early loss in production of the CD4 cytokines IL-2 and IFN-gamma was correlated with an increase in the B cell stimulatory cytokines IL-4, IL-5, and IL-10. We therefore assessed the production of IL-4 generated by PBL from HIV-seropositive (HIV+) individuals who did not have AIDS, yet who exhibited different TH functional categories based on their IL-2 production profiles. We observed that the decreases in recall antigen-stimulated IL-2 production were accompanied by an increase in IL-4 production. The loss of recall antigen-stimulated responses in HIV+ individuals could be reversed in vitro by anti-IL-4 antibody. Our results suggest that the TH functions assessed by IL-4 production replace the normally dominant TH function of antigen-stimulated IL-2 production in the progression toward AIDS, and raise the possibility of cytokine cross-regulation in AIDS therapy. | lld:pubmed |
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| pubmed-article:8450057 | pubmed:language | eng | lld:pubmed |
| pubmed-article:8450057 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8450057 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:8450057 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8450057 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:8450057 | pubmed:issn | 0021-9738 | lld:pubmed |
| pubmed-article:8450057 | pubmed:author | pubmed-author:ShearerG MGM | lld:pubmed |
| pubmed-article:8450057 | pubmed:author | pubmed-author:ClericiMM | lld:pubmed |
| pubmed-article:8450057 | pubmed:author | pubmed-author:WynnT ATA | lld:pubmed |
| pubmed-article:8450057 | pubmed:author | pubmed-author:HendrixC WCW | lld:pubmed |
| pubmed-article:8450057 | pubmed:author | pubmed-author:VenzonD JDJ | lld:pubmed |
| pubmed-article:8450057 | pubmed:author | pubmed-author:HakimF TFT | lld:pubmed |
| pubmed-article:8450057 | pubmed:author | pubmed-author:BlattSS | lld:pubmed |
| pubmed-article:8450057 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:8450057 | pubmed:volume | 91 | lld:pubmed |
| pubmed-article:8450057 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:8450057 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:8450057 | pubmed:pagination | 759-65 | lld:pubmed |
| pubmed-article:8450057 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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