pubmed-article:10491413 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:10491413 | lifeskim:mentions | umls-concept:C0332307 | lld:lifeskim |
pubmed-article:10491413 | lifeskim:mentions | umls-concept:C0214743 | lld:lifeskim |
pubmed-article:10491413 | lifeskim:mentions | umls-concept:C0239946 | lld:lifeskim |
pubmed-article:10491413 | lifeskim:mentions | umls-concept:C1155266 | lld:lifeskim |
pubmed-article:10491413 | lifeskim:mentions | umls-concept:C1527148 | lld:lifeskim |
pubmed-article:10491413 | lifeskim:mentions | umls-concept:C1999216 | lld:lifeskim |
pubmed-article:10491413 | lifeskim:mentions | umls-concept:C1533157 | lld:lifeskim |
pubmed-article:10491413 | pubmed:issue | 6 | lld:pubmed |
pubmed-article:10491413 | pubmed:dateCreated | 1999-10-13 | lld:pubmed |
pubmed-article:10491413 | pubmed:abstractText | In schistosomiasis, chronic parasite egg-induced granuloma formation can lead to tissue destruction and fibrosis, which causes much of the morbidity and mortality associated with this disease. Here we show the importance of IL-13 in the pathogenesis of schistosomiasis, and demonstrate, perhaps for the first time, the therapeutic efficacy of an IL-13 inhibitor, sIL-13Ralpha2-Fc, in the control of hepatic fibrosis. T-helper type 2 (Th2) cytokines dominate the immune response in mice infected with Schistosoma mansoni, yet the specific contributions of IL-13 and IL-4 to the development of fibrosis were not previously investigated. Our studies demonstrate that both cytokines play redundant roles in granuloma formation, which explains the ability of IL-4-deficient mice to form granulomas around eggs. More importantly, however, these studies demonstrate that IL-13 is the dominant Th2-type cytokine regulating fibrosis. IL-13 stimulated collagen production in fibroblasts, and procollagen I and procollagen III mRNA expression was decreased in sIL-13Ralpha2-Fc-treated mice. Moreover, the reduction in fibrosis observed in IL-4-deficient mice was much less pronounced than that in sIL-13Ralpha2-Fc-treated animals. Fibrosis is a major pathological manifestation of a number of allergic, autoimmune, and infectious diseases. Thus, our findings provide evidence that IL-13 inhibitors may be of general therapeutic benefit in preventing damaging tissue fibrosis resulting from Th2-dominated inflammatory responses. | lld:pubmed |
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pubmed-article:10491413 | pubmed:language | eng | lld:pubmed |
pubmed-article:10491413 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10491413 | pubmed:citationSubset | AIM | lld:pubmed |
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pubmed-article:10491413 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:10491413 | pubmed:month | Sep | lld:pubmed |
pubmed-article:10491413 | pubmed:issn | 0021-9738 | lld:pubmed |
pubmed-article:10491413 | pubmed:author | pubmed-author:CheeverA WAW | lld:pubmed |
pubmed-article:10491413 | pubmed:author | pubmed-author:DonaldsonD... | lld:pubmed |
pubmed-article:10491413 | pubmed:author | pubmed-author:WynnT ATA | lld:pubmed |
pubmed-article:10491413 | pubmed:author | pubmed-author:ChiaramonteM... | lld:pubmed |
pubmed-article:10491413 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:10491413 | pubmed:volume | 104 | lld:pubmed |
pubmed-article:10491413 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:10491413 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:10491413 | pubmed:pagination | 777-85 | lld:pubmed |
pubmed-article:10491413 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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pubmed-article:10491413 | pubmed:year | 1999 | lld:pubmed |
pubmed-article:10491413 | pubmed:articleTitle | An IL-13 inhibitor blocks the development of hepatic fibrosis during a T-helper type 2-dominated inflammatory response. | lld:pubmed |
pubmed-article:10491413 | pubmed:affiliation | Schistosomiasis Immunology and Pathology Unit, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA. | lld:pubmed |
pubmed-article:10491413 | pubmed:publicationType | Journal Article | lld:pubmed |
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