The costimulatory signal CD28 is fully functional but cannot correct the impaired antigen response in T cells of patients with common variable immunodeficiency

The costimulatory signal CD28 is fully functional but cannot correct the impaired antigen response in T cells of patients with common variable immunodeficiency
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共刺激信号CD28功能齐全,但无法纠正普通变异性免疫缺陷患者T细胞中受损的抗原反应

DOI:
10.1111/j.1365-2249.1994.tb06512.x
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发表时间:
1994
影响因子:
4.6
通讯作者:
M. Eibl
M. Eibl
中科院分区:
医学3区
文献类型:
--
作者:
M. Fischer;H. Wolf;H. Eggenbauer;V. Thon;E. Vogel;J. Lokaj;J. Litzman;J. Mannhalter;M. Eibl

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广泛的不同免疫学异常被认为是导致特异性抗体产生受损和常见变异型免疫缺陷(CVID)中存在的所有或选定免疫球蛋白同种型减少的原因。这些异常包括受损的B细胞分化和/或功能、缺陷的巨噬细胞功能和显著的T细胞检测。本研究的目的是阐明辅助分子CD 28是否参与CVID患者T细胞抗原反应受损。我们的结果表明,CD 28共刺激在用抗CD 3或抗TCR单克隆抗体刺激的T细胞中是有功能的。但不能纠正患者外周血T细胞对破伤风类毒素的受损反应。对患者长期培养的T细胞的分析进一步证实了这些结果。外源性rIL-2(另一种共刺激物)增强了患者抗原驱动的外周血T淋巴细胞或长期培养的T细胞的增殖和淋巴因子产生缺陷,但并未纠正。这些发现表明,这些患者T细胞中的CD 28信号通路未受损,并且通过CD 28的共刺激无法纠正TCR介导的T细胞活化过程中发生的缺陷。
A wide spectrum of different immunologic abnormalities have been postulated as being responsible for the impairment of specific antibody production and the decrease in all or selected immunoglobulin isotypes present in common variable immunodeficiency (CVID). These abnormalities include impaired B cell differentiation and or function, defective macrophage function, and significant T cell detects. The aim of the present study was to delineate whether the accessory molecule CD28 is involved in the impaired antigen response of T cell from patients with CVID. Our results demonstrate that CD28 costimulation was functional in T cells stimulated with anti‐CD3 or anti‐TCR MoAb. but could not correct the impaired response of patients' peripheral blood T cells to tetanus toxoid. Analysis of patients" long‐term cultured T cells further confirmed these results. Exogenous rIL‐2, another costimulus, augmented but did not correct the defective proliferation and lymphokine production in patients" antigen‐driven peripheral blood T lymphocytes or in long‐term cultured T cells. These findings indicate that the CD28 signalling pathway in these patients’T cells is unimpaired, and that costimulation via CD28 cannot correct the defect occurring in the course of TCR‐mediated T cell activation.
DOI: 10.4049/jimmunol.147.8.2461
发表时间: 1991-10
影响因子: 4.4
作者:
M. Jenkins;P. Taylor;S. Norton;K. Urdahl
通讯作者: M. Jenkins;P. Taylor;S. Norton;K. Urdahl
常见变异型免疫缺陷中的 T 细胞激活缺陷:通过佛波醇肉豆蔻酸酯乙酸酯 (PMA) 或同种异体巨噬细胞恢复。
DOI: 10.1016/0090-1229(87)90066-3
发表时间: 1987
期刊: Clinical immunology and immunopathology
影响因子: --
作者:
Fiedler,W;Sykora,KW;Welte,K;Kolitz,JE;Cunningham-Rundles,C;Holloway,K;Miller,GA;Souza,L;Mertelsmann,R
通讯作者: Mertelsmann,R