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类风湿性关节炎和骨关节炎中黏附分子CD66a、CD66b和CD31的滑膜表达增加。

Increased synovial expression of the adhesion molecules CD66a, CD66b, and CD31 in rheumatoid and osteoarthritis.

作者信息

Szekanecz Z, Haines G K, Harlow L A, Shah M R, Fong T W, Fu R, Lin S J, Koch A E

机构信息

Department of Medicine, Northwestern University Medical School, Chicago, Illinois 60611, USA.

出版信息

Clin Immunol Immunopathol. 1995 Aug;76(2):180-6. doi: 10.1006/clin.1995.1113.

Abstract

Leukocyte-endothelial interaction mediated by adhesion molecules may play a role in the ingress of inflammatory cells into the rheumatoid (RA) synovial tissue (ST). A number of these molecules have been shown to be up-regulated in the inflamed compared to normal ST. We studied the distribution of two members of the CD66 carcinoembryonic antigen adhesion molecule family, as well as that of CD31, an antigen structurally related to CD66, on various cell types in the RA compared to osteoarthritic (OA) and normal ST. Immunoperoxidase histochemistry was carried out using monoclonal antibodies to CD66a, CD66b, and CD31. This study was performed on ST from 10 patients with RA, 10 with OA, and 4 normal individuals. CD66a, and CD66b were expressed on RA and OA ST myeloid cells but not on normal ST lining cells and interstitial macrophages, suggesting that these antigens may be specific markers of diseased compared to normal ST macrophages (P < 0.05). CD31 was present on more RA and OA than on normal ST macrophages. Also, CD31 was present on most RA, OA, and normal ST endothelial cells. Our results indicate that the expression of CD66a, CD66b, and CD31, members of the immunoglobulin superfamily of adhesion receptors, is up-regulated on cells of myeloid origin in the inflamed compared to normal ST. These results suggest that the CD66 antigens and CD31 may be involved in the adhesive events in the inflamed synovium.

摘要

由黏附分子介导的白细胞-内皮细胞相互作用可能在炎性细胞进入类风湿性关节炎(RA)滑膜组织(ST)的过程中发挥作用。与正常ST相比,已证实许多此类分子在发炎的ST中上调。我们研究了CD66癌胚抗原黏附分子家族的两个成员以及与CD66结构相关的抗原CD31在RA与骨关节炎(OA)及正常ST的各种细胞类型上的分布情况。使用针对CD66a、CD66b和CD31的单克隆抗体进行免疫过氧化物酶组织化学分析。本研究对10例RA患者、10例OA患者和4例正常个体的ST进行。CD66a和CD66b在RA和OA的ST髓样细胞上表达,但在正常ST衬里细胞和间质巨噬细胞上不表达,这表明与正常ST巨噬细胞相比,这些抗原可能是患病的特异性标志物(P<0.05)。CD31在RA和OA的ST巨噬细胞上的表达多于正常ST。此外,大多数RA、OA和正常ST的内皮细胞上都有CD31。我们的结果表明,与正常ST相比,黏附受体免疫球蛋白超家族成员CD66a、CD66b和CD31在发炎的髓样来源细胞上的表达上调。这些结果表明,CD66抗原和CD31可能参与了发炎滑膜中的黏附事件。

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