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dc.contributor.authorBabaloo, Z
dc.contributor.authorKaye, PM
dc.contributor.authorEslami, MB
dc.date.accessioned2018-08-26T08:58:48Z
dc.date.available2018-08-26T08:58:48Z
dc.date.issued2001
dc.identifier.urihttp://dspace.tbzmed.ac.ir:8080/xmlui/handle/123456789/54738
dc.description.abstractThe role of interleukin (IL)-13, a Th2 cytokine sharing many of the features of IL-4, has not previously been examined in patients with visceral leishmaniasis (VL). We examined sera from Iranian patients with VL caused by Leishmania infantum. Serum IL-13 was detected in 50% (22/44) of patients with active primary disease. In comparison, IL-10 was detected in 79.5% (35/44), interferon ? (IFN?) in 38.5% (17/44), and IL-4 in only 5% (2/44) of these patients. With few exceptions all 3 cytokines were undetectable after clinical recovery following antimony therapy. Five of 7 patients (71%) who failed antimony therapy and had relapsing disease had similar levels of IL-10 to patients with active primary disease. However, with only 1 exception, IL-13, IFN? and IL-4 were not detected in such patients. These data suggest that relapsing disease may result from defective cellular immunity, unrelated to immunosuppression mediated by IL-10.
dc.language.isoEnglish
dc.relation.ispartofTransactions of the Royal Society of Tropical Medicine and Hygiene
dc.subjectantimony
dc.subjectcytokine
dc.subjectgamma interferon
dc.subjectinterleukin 10
dc.subjectinterleukin 13
dc.subjectinterleukin 4
dc.subjectarticle
dc.subjectblood analysis
dc.subjectcellular immunity
dc.subjectchild
dc.subjectcontrolled study
dc.subjectfemale
dc.subjecthuman
dc.subjecthuman cell
dc.subjectimmune deficiency
dc.subjectIran
dc.subjectLeishmania infantum
dc.subjectmajor clinical study
dc.subjectmale
dc.subjectnonhuman
dc.subjectrelapse
dc.subjectTh1 cell
dc.subjectTh2 cell
dc.subjecttreatment failure
dc.subjectvisceral leishmaniasis
dc.subjectIrania
dc.subjectLeishmania infantum
dc.subjectProtozoa
dc.titleInterleukin-13 in Iranian patients with visceral leishmaniasis: Relationship to other Th2 and Th1 cytokines
dc.typeArticle
dc.citation.volume95
dc.citation.issue1
dc.citation.spage85
dc.citation.epage88
dc.citation.indexScopus
dc.identifier.DOIhttps://doi.org/10.1016/S0035-9203(01)90344-X


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