Munson L G, Scott M E, Landay A L, Spear G T
Department of Immunology/Microbiology, Rush Medical School, Chicago, Illinois 60612.
Clin Immunol Immunopathol. 1995 Apr;75(1):20-5. doi: 10.1006/clin.1995.1047.
Previous studies have shown that complement receptor 1 (CR1) expression on erythrocytes is decreased under several conditions including HIV infection and autoimmune diseases. The goal of this study was to determine whether expression of CR1 on peripheral blood B cells, where this receptor plays a role during immune responses, is altered in persons with HIV infection. The B cells from rheumatoid arthritis (RA) patients were also assessed since this represents a group with known complement and B cell abnormalities. The CD19+ B cells from persons with either HIV infection or RA had significantly reduced levels of CR1 when compared with control donors (75 and 72% CR1+ versus 94% CR1+ for control donors). The reduction of B cell CR1 occurred in both the percentage of B cells positive for CR1 and the levels of CR1 found on positive cells. In contrast, CR1 on monocytes was not reduced. As shown in previous studies, CR2 was also found to be reduced on B cells from the HIV-infected persons and there was extensive overlap between the B cell subsets which lacked expression of CR1 and CR2. The complement receptor-negative B cells found in HIV-infected persons were not immature or activated as defined by their lack of expression of CD10 or B7, respectively. Elevated levels of C4d, a classical complement pathway-activation product, were detected in plasma from both HIV-infected and RA patients. These studies suggest that chronic complement activation occurring in persons with HIV infection or RA can affect the complement receptor phenotype of peripheral blood B cells. Since complement receptors are involved in activation of B cells, the subset that lacks CR1 may represent cells that have encountered immune complexes and may therefore be stimulated. Additionally, the downregulation of complement receptors may have significant effects on the ability of B cells to capture and present opsonized antigens.
先前的研究表明，在包括HIV感染和自身免疫性疾病在内的多种情况下，红细胞上的补体受体1（CR1）表达会降低。本研究的目的是确定在免疫反应中起作用的外周血B细胞上CR1的表达在HIV感染者中是否发生改变。由于类风湿性关节炎（RA）患者代表了一组已知存在补体和B细胞异常的人群，因此也对其B细胞进行了评估。与对照供体相比，HIV感染者或RA患者的CD19 + B细胞中CR1水平显著降低（对照供体的CR1 +为94%，而HIV感染者或RA患者分别为75%和72%）。B细胞CR1的减少既发生在CR1阳性B细胞的百分比上，也发生在阳性细胞上发现的CR1水平上。相比之下，单核细胞上的CR1没有减少。如先前研究所示，HIV感染者的B细胞上的CR2也被发现减少，并且缺乏CR1和CR2表达的B细胞亚群之间存在广泛重叠。在HIV感染者中发现的补体受体阴性B细胞，分别根据其缺乏CD10或B7的表达，并非未成熟或活化状态。在HIV感染者和RA患者的血浆中均检测到经典补体途径激活产物C4d水平升高。这些研究表明，HIV感染者或RA患者中发生的慢性补体激活可影响外周血B细胞的补体受体表型。由于补体受体参与B细胞的激活，缺乏CR1的亚群可能代表遇到免疫复合物并因此可能受到刺激的细胞。此外，补体受体的下调可能对B细胞捕获和呈递调理抗原的能力产生重大影响。
