Autoantibodies against CD4 cells are associated with CD4 helper defects in human immunodeficiency virus-infected patients.
Autoantibodies against CD4 cells are associated with CD4 helper defects in human immunodeficiency virus-infected patients.
复制标题
针对 CD4 细胞的自身抗体与人类免疫缺陷病毒感染患者的 CD4 辅助缺陷有关。
作者：
R. Weimer;V. Daniel;R. Zimmermann;K. Schimpf;G. Opelz
为探讨抗CD4阳性淋巴细胞自身抗体是否可能导致辅助性功能障碍，对61例血友病患者进行了自身抗体形成和T细胞功能检测。人类免疫缺陷病毒(HIV)阴性20例，HIV阳性CDC II或III期26例，HIV阳性CDC IV期15例。T淋巴细胞、CD4阳性或CD8阳性T细胞亚群与B淋巴细胞和商陆丝裂原(PWM)共培养6d，用反向溶血空斑试验检测Ig分泌细胞。用流式细胞仪分析T细胞或T亚群表面是否存在IgM、Ig G、C3d或gp120。在对照组或HIV阴性患者中没有检测到针对CD4+T细胞的自身抗体，但在HIV阳性患者中很常见(41例患者中有20例)。在有自身抗体的患者中，我们发现CD4辅助缺陷的发生率增加(在CDC II或III患者中P<0.0001；在CDC IV患者中P<0.02)。13例IgM自身抗体阳性患者中有12例存在CD4辅助缺陷，4例IgG自身抗体阳性患者中有4例存在辅助细胞缺陷。补体结合与此无关。针对CD4细胞的自身抗体的形成不是由于体内B细胞刺激的增加(自发斑块形成：自身抗体阴性患者中611+/-204 PFC/10(6)B细胞vv650+/-202 PFC/10(6)B细胞；不显着)。因此，我们的结果表明，自身抗体的形成不是由体内B细胞激活的一般状态引起的。相反，自身抗体的产生似乎与B细胞增殖或分化缺陷相一致，这在CDC II和III患者中表现为丝裂原刺激的B细胞反应减少(P<0.05)。抗CD4细胞自身抗体似乎参与了HIV感染患者的CD4辅助缺陷的发病机制。
To investigate whether autoantibodies against CD4-positive lymphocytes might induce helper dysfunction, autoantibody formation and T-cell function was examined simultaneously in 61 hemophilia patients. Twenty patients were human immunodeficiency virus (HIV)-negative, 26 HIV-positive stage CDC II or III, and 15 were HIV-positive stage CDC IV. T lymphocytes, CD4-positive, or CD8-positive T subsets were cocultured with B lymphocytes and pokeweed mitogen (PWM) for 6 days and Ig-secreting cells were assessed in a reverse hemolytic plaque assay. The presence of IgM, IgG, C3d, or gp120 on the surface of T cells or T subsets was analyzed by flow cytometry. Autoantibodies against CD4-positive T cells were not detected in controls or HIV-negative patients, but were common in HIV-positive patients (20 of 41 patients). In patients with autoantibodies we found an increased incidence of CD4 helper defects (P less than .0001 in CDC II or III patients; P less than .02 in CDC IV patients). 12 of 13 patients with IgM autoantibodies and 4 of 4 with IgG autoantibodies showed CD4 helper defects. Complement fixation had no relevance. Autoantibody formation against CD4 cells was not due to increased in vivo B-cell stimulation (spontaneous plaque formation: 611 +/- 204 PFC/10(6) B cells in autoantibody-negative patients v 650 +/- 202 PFC/10(6) B cells in autoantibody-positive patients; not significant). Thus, our results suggest that autoantibody formation is not caused by a general state of in vivo B-cell activation. Rather, the production of autoantibodies appears to coincide with defects in B-cell proliferation or differentiation, as shown by reduced mitogen-stimulated B-cell responses in CDC II and III patients (P less than .05). Autoantibodies against CD4 cells appear to be involved in the pathogenesis of CD4 helper defects of HIV-infected patients.
患有免疫性血小板减少症的同性恋男性的目标血小板抗原。
DOI：
10.1056/nejm198511283132202
发表时间：
1985
期刊：
The New England journal of medicine
影响因子：
--
作者：
Stricker,RB;Abrams,DI;Corash,L;Shuman,MA
通讯作者：
Shuman,MA
获得性免疫缺陷综合征 (AIDS) 患者血清中针对非 HLA 抗原的淋巴细胞毒性抗体。
DOI：
--
发表时间：
1983
期刊：
Progress in clinical and biological research
影响因子：
--
作者：
Pollack,MS;Callaway,C;LeBlanc,D;Robinson,HM;Mastrota,F;Dupont,B;Koziner,B
通讯作者：
Koziner,B
人类免疫缺陷病毒对正常 B 淋巴细胞的刺激和抑制影响。
DOI：
10.1073/pnas.83.23.9124
发表时间：
1986
影响因子：
11.1
作者：
Pahwa,S;Pahwa,R;Good,RA;Gallo,RC;Saxinger,C
通讯作者：
Saxinger,C