| pubmed-article:3487507 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:3487507 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:3487507 | lifeskim:mentions | umls-concept:C0343900 | lld:lifeskim |
| pubmed-article:3487507 | lifeskim:mentions | umls-concept:C1522405 | lld:lifeskim |
| pubmed-article:3487507 | lifeskim:mentions | umls-concept:C1817908 | lld:lifeskim |
| pubmed-article:3487507 | lifeskim:mentions | umls-concept:C1709059 | lld:lifeskim |
| pubmed-article:3487507 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:3487507 | pubmed:dateCreated | 1986-8-11 | lld:pubmed |
| pubmed-article:3487507 | pubmed:abstractText | Depression of the cellular immune responses in mice with disseminated histoplasmosis is associated with deficient production of interleukin-2 (IL-2) by splenocytes. Therefore, we examined whether a highly purified preparation of IL-2, recombinant human IL-2 (rIL-2), could modify the cellular immune responses in infected mice and whether this lymphokine could alter the severity of histoplasmosis in animals. Exogenous rIL-2, at concentrations of up to 1,000 U/ml, failed to augment the proliferative responses to concanavalin A by unfractionated splenocytes or splenic T cells from mice infected for 1 week. In addition, rIL-2 did not modulate the plaque-forming cell response to sheep erythrocytes by splenocytes from these same mice. However, at week 3, rIL-2 in concentrations ranging from 10 to 1,000 U/ml considerably augmented the proliferative response to concanavalin A and plaque-forming cell response to sheep erythrocytes by splenocytes from infected mice. Kinetics studies demonstrated that rIL-2 exerted maximal immunoregulatory activity when added on day 0 or 1 to cultures of splenocytes. In vivo administration of rIL-2, 200 to 20,000 U/day, for 10 days to normal and 3-week-infected mice did not alter the proliferative activity of splenocytes to concanavalin A; 200,000 U of rIL-2 per day actually depressed the proliferative responses of splenocytes from normal and infected mice. In vivo, rIL-2 did not modify delayed-type hypersensitivity responses to sheep erythrocytes or to histoplasmin by normal and infected mice. Moreover, treatment with rIL-2 in vivo did not reduce the number of Histoplasma CFU in spleens of mice. Thus, despite the immunoenhancing effect of rIL-2 in vitro, this lymphokine failed to exert similar effects in vivo. | lld:pubmed |
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| pubmed-article:3487507 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:3487507 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:3487507 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:3487507 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:3487507 | pubmed:issn | 0019-9567 | lld:pubmed |
| pubmed-article:3487507 | pubmed:author | pubmed-author:HarrisJ EJE | lld:pubmed |
| pubmed-article:3487507 | pubmed:author | pubmed-author:BullockW EWE | lld:pubmed |
| pubmed-article:3487507 | pubmed:author | pubmed-author:TaylorC LCL | lld:pubmed |
| pubmed-article:3487507 | pubmed:author | pubmed-author:DeepeG SGSJr | lld:pubmed |
| pubmed-article:3487507 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:3487507 | pubmed:volume | 53 | lld:pubmed |
| pubmed-article:3487507 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:3487507 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:3487507 | pubmed:pagination | 6-12 | lld:pubmed |
| pubmed-article:3487507 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:3487507 | pubmed:meshHeading | pubmed-meshheading:3487507-... | lld:pubmed |
| pubmed-article:3487507 | pubmed:year | 1986 | lld:pubmed |
| pubmed-article:3487507 | pubmed:articleTitle | Modulation of cellular immune responses in mice with disseminated histoplasmosis by recombinant interleukin-2. | lld:pubmed |
| pubmed-article:3487507 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:3487507 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:3487507 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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