کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9244064 | 1209899 | 2005 | 12 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Cdcs1, a Major Colitogenic Locus in Mice, Regulates Innate and Adaptive Immune Response to Enteric Bacterial Antigens
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کلمات کلیدی
BMDMGBP1NFKB1NOD2/CARD15BMDCT helperMDPmuramyl dipeptideTNFEMSALTANF-κBTLRoligodeoxynucleotideODNC3HAPCC3H/HeJ - C3H / HEJcDCs - cdc هاElectrophoretic mobility shift assay - آزمون تحرک تحرک الکتروفورزantigen-presenting cell - آنتیژن ارائه سلولlipoteichoic acid - اسید لیپتویکوئیکinterferon - اینترفرونIFN - اینترفرون هاinterleukin - اینترلوکینToll-like receptor - تیالآرBone marrow–derived dendritic cell - سلول های دندانیایی حاصل از استخوان مغز استخوانtumor necrosis factor - فاکتور نکروز تومورnuclear factor-κB - فاکتور هسته ای κBBone marrow–derived macrophage - ماکروفاژ حاصل از استخوان مغز استخوانRANTES - مطالب
موضوعات مرتبط
علوم پزشکی و سلامت
پزشکی و دندانپزشکی
بیماریهای گوارشی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Background & Aims: The absence of interleukin 10, a key cytokine in gut homeostasis, causes severe colitis in C3H/HeJBir but not C57BL/6J mice. The major modifier for colitis was mapped on chromosome 3 and designated cytokine deficiency-induced colitis susceptibility 1 (Cdcs1). We developed reciprocal Cdcs1 congenic stocks on both interleukin 10-deficient backgrounds to identify the susceptibility gene and its function. Methods: C3H/HeJBir congenic for the C57BL/6J-derived Cdcs1 allele and reciprocal C57BL/6J congenic for the C3H/HeJBir allele were analyzed for colitis development. Parental strains were compared by electrophoretic mobility shift assay to assess the candidacy of nuclear factor-κB p50 in the Cdcs1 interval. Functional differences were observed in innate and adaptive immune responses of parental and congenic stocks after bacterial ligand exposure in vitro (cytokine release from bone marrow-derived macrophage and dendritic cells) and in vivo (serum cytokines and primed CD4+ T cell proliferation). Results: Cdcs1 was positioned within a minimum 7-megabase interval containing nuclear factor-κB p50. C3H/HeJBir colitis was significantly diminished by the C57BL/6J genome in this interval. Conversely, colitis in C57BL/6J was significantly exacerbated by the reciprocal C3H/HeJBir genome. C3H/HeJBir macrophages constitutively expressed higher nuclear factor-κB p50. Functional assays showed that C3H/HeJBir showed reduced innate responsiveness both in vivo and in vitro to bacterial ligands but showed increased CD4 T-cell responses compared with C57BL/6J. This differential responsiveness was controlled by the respective allele at Cdcs1. Conclusions: The colitogenic Cdcs1 allele impairs innate immunity to bacterial products and in turn skews the adaptive immune response toward compensatory hyperresponsiveness and chronic intestinal inflammation.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Gastroenterology - Volume 129, Issue 5, November 2005, Pages 1473-1484
Journal: Gastroenterology - Volume 129, Issue 5, November 2005, Pages 1473-1484
نویسندگان
Jason Beckwith, Yingzi Cong, John P. Sundberg, Charles O. Elson, Edward H. Leiter,