TNF signals are dispensable for the generation of CD23+CD21/35-high CD1d-high B cells in inflamed lymph nodes

被引：6

作者：

Kuzin, Igor I. ^{[1
]}

Bouta, Echoe M. ^{[2
,3
]}

Schwarz, Edward M. ^{[2
,3
]}

Bottaro, Andrea ^{[1
]}

机构：

[1] Rowan Univ, Dept Biomed Sci, Cooper Med Sch, Camden, NJ USA

[2] Univ Rochester, Sch Med & Dent, Dept Biomed Engn, Ctr Musculoskeletal Res, Rochester, NY USA

[3] Univ Rochester, Sch Med & Dent, Dept Orthopaed, Rochester, NY USA

来源：

CELLULAR IMMUNOLOGY | 2015年 / 296卷 / 02期

关键词：

B cells; Lymph nodes; Inflammation; Tumor necrosis factor; INFLAMMATORY ARTHRITIS; RHEUMATOID-ARTHRITIS; TRANSGENIC MICE; THERAPY; HOMEOSTASIS; TARGETS; GROWTH; FLARE; MODEL;

D O I：

10.1016/j.cellimm.2015.04.005

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Tumor necrosis factor (TNF) is a key cytokine in rheumatoid arthritis (RA) pathogenesis, as underscored by the clinical effectiveness of TNF antagonists. While several of TNF's key targets in RA are well understood, its many pleiotropic effects remain to be elucidated. TNF-transgenic mice develop inflammatory-erosive arthritis associated with disruption of draining lymph node histology and function, and accumulation of B cells with unique phenotypic and functional features consistent with contribution to pathogenesis (B cells in inflamed nodes, Bin). Bin cell induction depends on the inflamed microenvironment, but the specific signals are unknown. Using anti-TNF treatment and TNF-receptor-deficient mice, here we show that Bin cells are induced and maintained independently of B cell-intrinsic TNF signals. (C) 2015 Elsevier Inc. All rights reserved.

引用

页码：133 / 137

页数：5

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