کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6119203 | 1592286 | 2015 | 16 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Distinct and synergistic roles of FcγRIIB deficiency and 129 strain-derived SLAM family proteins in the development of spontaneous germinal centers and autoimmunity
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کلمات کلیدی
PNASRBCCFSETFHanti-nuclear antibody - آنتی بادی ضد هسته ایpeanut agglutinin - آگلوتینین بادام زمینیSLAM - اسلامهANA - اصلیautoimmunity - خودایمنیB cells - سلول های BFollicular helper T cells - سلول های T کمکی به فولیکول هاSystemic lupus erythematosus - لوپوس اریتماتوی سیستمیکSLE - لوپوس منتشر یا لوپوس اریتماتوس سیستمیکGerminal centers - مراکز گیاهیGerminal center - مرکز ژرمینالsignaling lymphocyte activation molecule - مولکول فعال سازی لنفوسیت سیگنالینگcarboxyfluorescein succinimidyl ester - کربوکسیفلوورسسین سوکسینیمیدیل استرsheep red blood cells - گلبول های قرمز گوسفند
موضوعات مرتبط
علوم زیستی و بیوفناوری
ایمنی شناسی و میکروب شناسی
ایمونولوژی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Distinct and synergistic roles of FcγRIIB deficiency and 129 strain-derived SLAM family proteins in the development of spontaneous germinal centers and autoimmunity Distinct and synergistic roles of FcγRIIB deficiency and 129 strain-derived SLAM family proteins in the development of spontaneous germinal centers and autoimmunity](/preview/png/6119203.png)
چکیده انگلیسی
The inhibitory IgG Fc receptor (FcγRIIB) deficiency and 129 strain-derived signaling lymphocyte activation molecules (129-SLAMs) are proposed to contribute to the lupus phenotype in FcγRIIB-deficient mice generated using 129 ES cells and backcrossed to C57BL/6 mice (B6.129.RIIBKO). In this study, we examine the individual contributions and the cellular mechanisms by which FcγRIIB deficiency and 129-derived SLAM family genes promote dysregulated spontaneous germinal center (Spt-GC) B cell and follicular helper T cell (Tfh) responses in B6.129.RIIBKO mice. We find that B6 mice congenic for the 129-derived SLAM locus (B6.129-SLAM) and B6 mice deficient in FcγRIIB (B6.RIIBKO) have increased Spt-GC B cell responses compared to B6 controls but significantly lower than B6.129.RIIBKO mice. These data indicate that both FcγRIIB deficiency and 129-SLAMs contribute to elevated Spt-GC B cell responses in B6.129.RIIBKO mice. However, only 129-SLAMs contribute significantly to augmented Tfh responses in B6.129.RIIBKO mice, and do so by a combination of T cell-dependent effects and enhanced B cell and DC-dependent antigen presentation to T cells. Elevated Spt-GC B cell responses in mice with FcγRIIB deficiency and polymorphic 129-SLAMs were associated with elevated metabolic activity, improved GC B cell survival and increased differentiation of naïve B cells into GC B cell phenotype. Our data suggest that the interplay between 129-SLAM expression on B cells, T cells and DCs is central to the alteration of the GC tolerance checkpoint, and that deficiency of FcγRIIB on B cells is necessary to augment Spt-GC responses, pathogenic autoantibodies, and lupus disease.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Autoimmunity - Volume 63, September 2015, Pages 31-46
Journal: Journal of Autoimmunity - Volume 63, September 2015, Pages 31-46
نویسندگان
Chetna Soni, Phillip P. Domeier, Eric B. Wong, Shwetank Shwetank, Tahsin N. Khan, Melinda J. Elias, Stephanie L. Schell, Aron E. Lukacher, Timothy K. Cooper, Ziaur S.M. Rahman,