| pubmed-article:10384133 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:10384133 | lifeskim:mentions | umls-concept:C0030664 | lld:lifeskim |
| pubmed-article:10384133 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:10384133 | lifeskim:mentions | umls-concept:C0021758 | lld:lifeskim |
| pubmed-article:10384133 | lifeskim:mentions | umls-concept:C0024297 | lld:lifeskim |
| pubmed-article:10384133 | lifeskim:mentions | umls-concept:C0123771 | lld:lifeskim |
| pubmed-article:10384133 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
| pubmed-article:10384133 | lifeskim:mentions | umls-concept:C1979963 | lld:lifeskim |
| pubmed-article:10384133 | lifeskim:mentions | umls-concept:C1979874 | lld:lifeskim |
| pubmed-article:10384133 | lifeskim:mentions | umls-concept:C1314677 | lld:lifeskim |
| pubmed-article:10384133 | lifeskim:mentions | umls-concept:C2003903 | lld:lifeskim |
| pubmed-article:10384133 | lifeskim:mentions | umls-concept:C0439667 | lld:lifeskim |
| pubmed-article:10384133 | lifeskim:mentions | umls-concept:C2911684 | lld:lifeskim |
| pubmed-article:10384133 | lifeskim:mentions | umls-concept:C0185117 | lld:lifeskim |
| pubmed-article:10384133 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:10384133 | pubmed:dateCreated | 1999-7-15 | lld:pubmed |
| pubmed-article:10384133 | pubmed:abstractText | Th2 lymphocytes have been postulated to play a major role in the immunopathology induced by Schistosoma mansoni infection. Nevertheless, infected IL-4 knockout (KO) and wild-type (wt) mice develop egg granulomas comparable in size. To further investigate the function of the Th2 response in egg pathology we studied IL-4Ralpha-deficient mice, which are nonresponsive to both IL-4 and IL-13. In striking contrast to IL-4 KO animals, infected IL-4Ralpha KO mice developed only minimal hepatic granulomas and fibrosis despite the presence of CD3+ T cells in the residual egg lesions. Moreover, liver lymphokine mRNA levels in these animals and IL-4 KO mice were equivalent. In addition, infected IL-4Ralpha-deficient, IL-4-deficient, and wt animals developed similar egg Ag-specific IgG Ab titers, arguing that CD4-dependent Th activity is intact in KO mice. As expected, IFN-gamma secretion was strongly up-regulated in mesenteric lymph node cultures from both groups of deficient animals, a change reflected in increased serum IgG2a and IgG2b Ab levels. Surprisingly, Th2 cytokine production in infected IL-4Ralpha KO mice was not abolished but was only reduced and resembled that previously documented in IL-4 KO animals. This residual Th2 response is likely to explain the ability of IL-4 KO mice to generate egg granulomas, which cannot be formed in IL-4Ralpha-deficient animals because of their lack of responsiveness to the same cytokine ligands. Taken together, these findings argue that tissue pathology in schistosomiasis requires, in addition to egg-specific CD4+ lymphocytes, a previously unrecognized IL-4Ralpha+ non-T cell effector population. | lld:pubmed |
| pubmed-article:10384133 | pubmed:language | eng | lld:pubmed |
| pubmed-article:10384133 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10384133 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:10384133 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:10384133 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10384133 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:10384133 | pubmed:issn | 0022-1767 | lld:pubmed |
| pubmed-article:10384133 | pubmed:author | pubmed-author:WardJ MJM | lld:pubmed |
| pubmed-article:10384133 | pubmed:author | pubmed-author:PaulW EWE | lld:pubmed |
| pubmed-article:10384133 | pubmed:author | pubmed-author:SherAA | lld:pubmed |
| pubmed-article:10384133 | pubmed:author | pubmed-author:CheeverA WAW | lld:pubmed |
| pubmed-article:10384133 | pubmed:author | pubmed-author:CasparPP | lld:pubmed |
| pubmed-article:10384133 | pubmed:author | pubmed-author:KullbergM CMC | lld:pubmed |
| pubmed-article:10384133 | pubmed:author | pubmed-author:JankovicDD | lld:pubmed |
| pubmed-article:10384133 | pubmed:author | pubmed-author:Noben-TrauthN... | lld:pubmed |
| pubmed-article:10384133 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10384133 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:10384133 | pubmed:volume | 163 | lld:pubmed |
| pubmed-article:10384133 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:10384133 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:10384133 | pubmed:pagination | 337-42 | lld:pubmed |
| pubmed-article:10384133 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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| pubmed-article:10384133 | pubmed:year | 1999 | lld:pubmed |
| pubmed-article:10384133 | pubmed:articleTitle | Schistosome-infected IL-4 receptor knockout (KO) mice, in contrast to IL-4 KO mice, fail to develop granulomatous pathology while maintaining the same lymphokine expression profile. | lld:pubmed |
| pubmed-article:10384133 | pubmed:affiliation | Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892, USA. djankovic@atlas.niaid.nih.gov | lld:pubmed |
| pubmed-article:10384133 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:10384133 | pubmed:publicationType | Comparative Study | lld:pubmed |
| pubmed-article:10384133 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| entrez-gene:16190 | entrezgene:pubmed | pubmed-article:10384133 | lld:entrezgene |
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