کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10941120 | 1095601 | 2012 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
IL-12 inhibits the TGF-β-dependent T cell developmental programs and skews the TGF-β-induced differentiation into a Th1-like direction
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کلمات کلیدی
TregsC-C chemokine receptor type 5TGF-βLipopolysacharidenTregsiTregsinduced regulatory T cellsRORγtConAIL-12CFSECCR5IFN-γPBSConcanavalin ALPSmAbFOXP3Monoclonal antibody - آنتی بادی مونوکلونالinterferon γ - اینترفرون γinterleukin-12 - اینترلوکین -12Transforming growth factor β - تبدیل فاکتور رشد βT cell differentiation - تمایز سلول Tforkhead box P3 - جعبه جعبه P3T cell subsets - زیر مجموعه های سلول TTh17 cells - سلول های Th17Helper T cell - سلول کمک کنندهRegulatory T cells - سلولهای تی تنظیمکنندهCytokines - سیتوکین هاphycoerythrin - فایکوئیریدینPhosphate buffered saline - فسفات بافر شورNitric oxide - نیتریک اکسیدcarboxyfluorescein succinimidyl ester - کربوکسیفلوورسسین سوکسینیمیدیل استر
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیولوژی سلول
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
The development and differentiation of T helper (Th) cell subsets is a highly plastic process which is strictly regulated by cytokines. Here we show that the transforming growth factor β (TGF-β)-dependent differentiation programs are negatively regulated by interleukin-12 (IL-12). The development of TGF-β-induced regulatory T cells (iTregs) or TGF-β/IL-6 activated Th17 cells from purified mouse CD4+CD25â T cells, stimulated with monoclonal antibody anti-CD3, was abrogated in the presence of IL-12 and a different developmental program was established. On the molecular level, IL-12 inhibited the expression of the lineage specific transcription factors Foxp3 and RORγt in developing Tregs and Th17 cells, respectively. Moreover, IL-12 was able to alter the development of iTregs and Th17 cells even when added to the differentiating cells after 48 h of the culture. The cells activated in the presence of TGF-β and IL-12 had an increased expression of the Th1 transcription factor T-bet, produced Th1 cytokines interferon γ and IL-2 and expressed IL-18 receptor and C-C chemokine receptor type 5 which are the phenotypic markers characteristic for Th1 cells. Furthermore, the cells activated in the presence of both TGF-β and IL-12, and not of TGF-β only, stimulated macrophages to produce nitric oxide. Altogether, these results indicate that IL-12 is a superior cytokine that has the ability to skew the already ongoing TGF-β-dependent iTreg or Th17 developmental program into Th1-like direction.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Immunobiology - Volume 217, Issue 1, January 2012, Pages 74-82
Journal: Immunobiology - Volume 217, Issue 1, January 2012, Pages 74-82
نویسندگان
Jana Prochazkova, Katerina Pokorna, Vladimir Holan,