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一名感染人类免疫缺陷病毒的类风湿关节炎患者的进行性关节破坏。

Progressive joint destruction in a human immunodeficiency virus-infected patient with rheumatoid arthritis.

作者信息

Müller-Ladner U, Kriegsmann J, Gay R E, Koopman W J, Gay S, Chatham W W

机构信息

University of Alabama at Birmingham 35294-0006, USA.

出版信息

Arthritis Rheum. 1995 Sep;38(9):1328-32. doi: 10.1002/art.1780380922.

Abstract

This article reports the case of a 63-year-old patient with rheumatoid arthritis (RA) whose symptoms of RA improved after the occurrence of a secondary human immunodeficiency virus (HIV) infection; however, the HIV infection did not affect the histologic parameters of joint destruction to the same extent as it did the clinical symptoms. Histologic and immunohistologic joint examinations of this patient revealed an ongoing production of cartilage- and bone-degrading enzymes by macrophages and fibroblasts, without the presence of T cells. These findings demonstrate that progressive joint destruction in RA can occur in the absence of T cells. Moreover, our results support the hypothesis that both T cell-dependent and T cell-independent pathways play a significant role in the pathogenesis of RA.

摘要

本文报道了一名63岁类风湿关节炎(RA)患者的病例,该患者在继发人类免疫缺陷病毒(HIV)感染后,RA症状有所改善;然而,HIV感染对关节破坏组织学参数的影响程度与对临床症状的影响程度不同。对该患者进行的组织学和免疫组织学关节检查显示,巨噬细胞和成纤维细胞持续产生降解软骨和骨的酶,且不存在T细胞。这些发现表明,RA中进行性关节破坏可在无T细胞的情况下发生。此外,我们的结果支持这样一种假说,即T细胞依赖性和T细胞非依赖性途径在RA发病机制中均起重要作用。

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