Expression of CD40 and CD40 ligand among cell populations within rheumatoid synovial compartment
Expression of CD40 and CD40 ligand among cell populations within rheumatoid synovial compartment
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DOI：
10.3109/08916930109001958
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发表时间：
2001-01-01
期刊：
影响因子：
3.5
通讯作者：
Lei, HY
中科院分区：
文献类型：
--
作者：
Liu, MF;Chao, SC;Lei, HY
最近有报道称，在人狼疮患者的淋巴样细胞中CD40配体（CD40L）的表达增强和延长，提示CD40/CD40L通路参与了系统性自身免疫性疾病的发病机制。因此，本研究旨在研究类风湿关节炎（RA）患者炎症关节内细胞群中CD40和CD40L的表达。结果显示，滑膜液（SF）中多数B细胞和单核细胞表达CD40。培养的滑膜成纤维细胞CD40也呈阳性。关于CD40L，我们发现T细胞和B细胞都可以表达CD40L。与正常对照组相比，RA患者CD40L(+) T细胞（8.71 +/- 17.69% vs 1.74 +/- 2.30%, P < 0.05）和CD40L(+)B细胞（7.71 +/- 7.64% vs 1.12 +/- 1.59% P < 0.05）水平较高。体外刺激后，RA患者T细胞的CD40L表达高于正常外周血T细胞。为了研究滑膜成纤维细胞表达CD40对关节间室tnf - α产生的影响，我们使用抗CD40抗体将CD40结合成纤维细胞1小时，然后与滑膜液单核细胞共培养。我们发现，在抗cd40抗体存在下，tnf - α水平下降。我们得出结论，类风湿关节内的淋巴样细胞存在CD40L的内在高表达，滑膜成纤维细胞可能通过表面CD40分子参与关节炎症。
Augmented and prolonged expression of CD40 ligand (CD40L) was recently reported in lymphoid cells from human lupus patients, suggesting that CD40/CD40L pathway was involved in the pathogenesis of systemic autoimmune diseases. This study was thus designed to study the expression of CD40 and CD40L among cell populations within inflammatory joints of patients with rheumatoid arthritis (RA). The result showed that most B cells and monocytes in synovial fluids (SF) expressed CD40. Cultured synovial fibroblasts also stained positive for CD40. Regarding CD40L, we found that T cells as well as B cells could express CD40L. Compared with normal controls, RA patients had higher levels of CD40L(+) T cells (8.71 +/- 17.69% vs 1.74 +/- 2.30 %, P > 0.05) and CD40L(+)B cells (7.71 +/- 7.64% vs 1.12 +/- 1.59% P < 0.05). After in vitro stimulation, T cells from RA patients had higher and longer CD40L expression than T cells from normal peripheral blood. For investigating the effect of CD40 expressed on synovial fibroblasts on TNF-alpha production in joint compartment, we used anti-CD40 antibody to bind CD40 on fibroblasts for one hour and then co-cultured with synovial fluid mononuclear cells. We found that the levels of TNF-alpha decreased in the presence of anti-CD40 antibody. We concluded that there was an intrinsic hyperexpression of CD40L on lymphoid cells within rheumatoid joints, and synovial fibroblasts could contribute to articular inflammation through surface CD40 molecule.