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瘤型麻风病中CD2的表达及功能

CD2 expression and function in lepromatous leprosy.

作者信息

Wong L, Salgame P, Torigian V K, Fu T H, Rea T H, Modlin R L

机构信息

Section of Dermatology, University of Southern California School of Medicine, Los Angeles 90033.

出版信息

Infect Immun. 1989 Sep;57(9):2815-9. doi: 10.1128/iai.57.9.2815-2819.1989.

DOI:10.1128/iai.57.9.2815-2819.1989
PMID:2474503
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC313532/
Abstract

Leprosy is a spectral disease in which clinical presentation is thought to be related to the host immune response. Previous investigations have suggested that selective unresponsiveness to Mycobacterium leprae in patients with lepromatous leprosy is due to the presence of M. leprae-specific T-suppressor cells. However, it has recently been suggested that CD2 modulation was the mechanism for the observed impaired immune response in lepromatous patients. Therefore, we studied the expression of CD2 and CD3 on lymphocytes in lepromatous skin lesions and peripheral blood mononuclear cells (PBMC). Using immunohistochemical techniques, we found that virtually all of the CD3+ cells in leprosy skin lesions expressed CD2. In addition, indirect immunofluorescence flow cytometry demonstrated that most CD3+ cells in the peripheral blood possessed the CD2 marker, suggesting that CD2 expression of T-lymphocytes is normal. T-cell activation using paired anti-T11(2) and anti-T11(3) or anti-CD3 monoclonal antibodies demonstrated similar 3H-thymidine incorporation and gamma interferon production in the PBMC of lepromatous patients in comparison with the PBMC of their contacts and tuberculoid patients. However, lepromatous PBMC did not proliferate or produce gamma interferon in response to M. leprae. Our data suggest not only that CD2 expression is normal on T lymphocytes in lepromatous leprosy skin lesions but also that CD2 expression in peripheral blood lymphocytes is functional in T-cell activation. Defective CD2 modulation does not appear to be the mechanism for specific unresponsiveness in lepromatous leprosy.

摘要

麻风是一种光谱疾病,其临床表现被认为与宿主免疫反应有关。先前的研究表明,瘤型麻风患者对麻风分枝杆菌的选择性无反应性是由于存在麻风分枝杆菌特异性T抑制细胞。然而,最近有人提出CD2调节是瘤型麻风患者免疫反应受损的机制。因此,我们研究了瘤型皮肤病变和外周血单个核细胞(PBMC)中淋巴细胞上CD2和CD3的表达。使用免疫组织化学技术,我们发现麻风皮肤病变中几乎所有的CD3+细胞都表达CD2。此外,间接免疫荧光流式细胞术表明外周血中大多数CD3+细胞具有CD2标记,这表明T淋巴细胞的CD2表达是正常的。使用配对的抗T11(2)和抗T11(3)或抗CD3单克隆抗体激活T细胞,结果显示与瘤型麻风患者的接触者和结核样型患者的PBMC相比,瘤型麻风患者的PBMC中3H-胸腺嘧啶核苷掺入和γ干扰素产生情况相似。然而,瘤型麻风患者的PBMC对麻风分枝杆菌没有增殖反应或产生γ干扰素。我们的数据不仅表明瘤型麻风皮肤病变中T淋巴细胞上的CD2表达正常,而且外周血淋巴细胞中的CD2表达在T细胞激活中具有功能。CD2调节缺陷似乎不是瘤型麻风特异性无反应性的机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/94a5/313532/bbf445617254/iai00069-0239-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/94a5/313532/bbf445617254/iai00069-0239-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/94a5/313532/bbf445617254/iai00069-0239-a.jpg

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