کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9245482 | 1209948 | 2005 | 13 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Colitis in mice lacking the common cytokine receptor γ chain is mediated by IL-6-producing CD4+ T cells
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کلمات کلیدی
FACSTNFmAbLCRFITCGAPDHTCrIL-6RTGFMonoclonal antibody - آنتی بادی مونوکلونالinterferon - اینترفرونIFN - اینترفرون هاinterleukin - اینترلوکینtransforming growth factor - تبدیل فاکتور رشدEnzyme-linked immunosorbent assay - تست الیزاELISA - تست الیزاCommon cytokine receptor γ chain - زنجیره γ گیرنده سیتوکین مشترکSpleen - طحالtumor necrosis factor - فاکتور نکروز تومورphycoerythrin - فایکوئیریدینfluorescein isothiocyanate - فلوئورسین ایسوتیوسیاناتfluorescence-activated cell sorter - فلورسانس فعال سلول مرتب سازLamina propria - لامینا پروپریاpolymerase chain reaction - واکنش زنجیره ای پلیمرازPCR - واکنش زنجیرهٔ پلیمرازglyceraldehyde-3-phosphate dehydrogenase - گلیسرالیدید-3-فسفات دهیدروژنازInterleukin-6 receptor - گیرنده اینترلوکین -6T-cell receptor - گیرنده لنفوسیت T
موضوعات مرتبط
علوم پزشکی و سلامت
پزشکی و دندانپزشکی
بیماریهای گوارشی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Colitis in mice lacking the common cytokine receptor γ chain is mediated by IL-6-producing CD4+ T cells Colitis in mice lacking the common cytokine receptor γ chain is mediated by IL-6-producing CD4+ T cells](/preview/png/9245482.png)
چکیده انگلیسی
Background & Aims: Mice that have a truncated mutation of the common cytokine receptor γ chain (CRγâ/Y) are known to spontaneously develop colitis. To identify the pathologic elements responsible for triggering this localized inflammatory disease, we elucidated and characterized aberrant T cells and their enteropathogenic cytokines in CRγâ/Y mice with colitis. Methods: The histologic appearance, cell population, T-cell receptor Vβ usage, and cytokine production of lamina propria lymphocytes were assessed. CRγâ/Y mice were treated with anti-interleukin (IL)-6 receptor monoclonal antibody to evaluate its ability to control colitis, and splenic CD4+ T cells from the same mouse model were adoptively transferred into SCID mice to see if they spurred the appearance of colitis. Results: We found marked thickening of the large intestine, an increase in crypt depth, and infiltration of the colonic lamina propria and submucosa with mononuclear cells in the euthymic CRγâ/Y mice, but not in the athymic CRγâ/Y mice, starting at the age of 8 weeks. Colonic CD4+ T cells with high expressions of antiapoptotic Bcl-x and Bcl-2 were found to use selected subsets (Vβ14) of T-cell receptor and to exclusively produce IL-6. Treatment of CRγâ/Y mice with anti-IL-6 receptor monoclonal antibody prevented the formation of colitis via the induction of apoptosis in IL-6-producing CD4+ T cells. Adoptive transfer of pathologic CD4+ T cells induced colitis in the recipient SCID mice. Conclusions: Colonic IL-6-producing thymus-derived CD4+ T cells are responsible for the development of colitis in CRγâ/Y mice.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Gastroenterology - Volume 128, Issue 4, April 2005, Pages 922-934
Journal: Gastroenterology - Volume 128, Issue 4, April 2005, Pages 922-934
نویسندگان
Yasuyuki Kai, Ichiro Takahashi, Hiromichi Ishikawa, Takachika Hiroi, Tsunekazu Mizushima, Chu Matsuda, Daisuke Kishi, Hiromasa Hamada, Hiroshi Tamagawa, Toshinori Ito, Kazuyuki Yoshizaki, Tadamitsu Kishimoto, Hikaru Matsuda, Hiroshi Kiyono,