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稳定表达B7抗原的A431角质形成细胞的辅助和同种异体抗原呈递细胞功能。

Accessory and alloantigen-presenting cell functions of A431 keratinocytes that stably express the B7 antigen.

作者信息

Gaspari A A, Ferbel B, Chen Z, Razvi F, Polakowska R

机构信息

Department of Dermatology, University of Rochester School of Medicine and Dentistry, New York 14627.

出版信息

Cell Immunol. 1993 Jul;149(2):291-302. doi: 10.1006/cimm.1993.1156.

Abstract

Because keratinocytes are tolerogenic antigen-presenting cells (APC), we investigated the role of B7/BB-1 in reconstituting defective accessory cell (AC) and APC functions by such nonlymphoid cells. KC were induced to stably express B7/BB-1 by DNA-mediated gene transfection. This single-transformed B7/BB-1+ A431 cell line (but not control A431) functioned as AC for lectin-induced T-cell proliferation, as well as oxidative mitogenesis. This costimulation was dependent on B7/BB-1 expression since the monoclonal antibody BB-1 blocked costimulation of PHA mitogenesis by 75%. After the induction of class II MHC antigen expression by interferon-gamma, B7/BB-1+ KC but not control KC presented alloantigens to resting T-cells in the primary mixed lymphocyte reaction. These data indicate that the stable expression of B7/BB-1 antigen by KC reconstitutes defective AC and alloantigen-presenting activity. The lack of expression of such second signal by normal KC may be responsible for their ability to induce clonal anergy in vitro and in vivo.

摘要

由于角质形成细胞是耐受性抗原呈递细胞(APC),我们研究了B7/BB-1在通过此类非淋巴细胞重建缺陷辅助细胞(AC)和APC功能中的作用。通过DNA介导的基因转染诱导角质形成细胞稳定表达B7/BB-1。这种单一转化的B7/BB-1+ A431细胞系(而非对照A431)作为AC参与凝集素诱导的T细胞增殖以及氧化有丝分裂。这种共刺激依赖于B7/BB-1的表达,因为单克隆抗体BB-1可阻断PHA有丝分裂75%的共刺激作用。在用干扰素-γ诱导II类MHC抗原表达后,B7/BB-1+角质形成细胞而非对照角质形成细胞在初次混合淋巴细胞反应中向静息T细胞呈递同种异体抗原。这些数据表明,角质形成细胞稳定表达B7/BB-1抗原可重建缺陷的AC和同种异体抗原呈递活性。正常角质形成细胞缺乏此类第二信号的表达可能是其在体内外诱导克隆无能的原因。

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