کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2429458 1106497 2012 9 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Chicken IL-17F: Identification and comparative expression analysis in Eimeria-infected chickens
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی زیست شناسی تکاملی
پیش نمایش صفحه اول مقاله
Chicken IL-17F: Identification and comparative expression analysis in Eimeria-infected chickens
چکیده انگلیسی

Interleukin-17F (IL-17F) is a proinflammatory cytokine, which plays an important role in gut homeostasis. A full-length chicken IL-17F (chIL-17F) cDNA with a 510-bp coding region was identified from ConA-activated chicken splenic lymphocytes. ChIL-17F shares 53% amino acid sequence identity with the previously described chicken IL-17 (chIL-17A) and 38–43% with mammalian homologues. The locus harboring chIL-17 and chIL-17F displayed inverted order compared to those of mammals. ChIL-17F transcript expression was high in lymphoblast cell line CU205 and at moderate levels in small and large intestines and liver. ChIL-17F and chIL-17 expression profiles were examined by quantitative real-time RT-PCR in mitogen-stimulated splenic lymphocytes and intestinal areas affected by Eimeria maxima and Eimeria tenella infections. Expression levels of chIL-17F, like chIL-17, were elevated in mitogen-activated splenic lymphocytes. ChIL-17F, but not chIL-17, expression was upregulated in intestinal tissues affected by E. maxima and E. tenella infections. Recombinant chIL-17F biological activities were similar to that of chIL-17 in primary chicken embryonic fibroblasts. These results suggest that chIL-17F is a unique member of the IL-17 family of cytokines.


► Chicken interleukin-17F was identified.
► The chIL-17F transcript was widely expressed, albeit at low levels, in most normal tissues.
► Recombinant chIL-17F biological activities were similar to that of chIL-17 in primary chicken embryonic fibroblasts.
► ChIL-17F, but not chIL-17, expression was upregulated in intestinal tissues affected by E. maxima and E. tenella infections.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Developmental & Comparative Immunology - Volume 38, Issue 3, November 2012, Pages 401–409
نویسندگان
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