Suppressor-cell antibody in systemic lupus erythematosus. Possible mechanism for suppressor-cell dysfunction.
Suppressor-cell antibody in systemic lupus erythematosus. Possible mechanism for suppressor-cell dysfunction.
复制标题
系统性红斑狼疮的抑制细胞抗体。
DOI：
--
复制
发表时间：
1979
影响因子：
15.9
通讯作者：
N. Abdou
中科院分区：
文献类型：
--
作者：
A. Sagawa;N. Abdou
对活动性系统性红斑狼疮（SLE）患者胸腺抑制性T细胞功能障碍的循环抗体进行了研究。将14例活动期和非活动期SLE患者的血清与22例正常血清进行比较。所有血清均用正常血小板池吸附，以排除抗组织相容性白细胞抗原抗体;用AB红细胞吸附，以排除同种血凝素;用正常骨髓来源（B）淋巴细胞、单核细胞和中性粒细胞池吸附，以清除抗B细胞抗体、Fc受体抗体和针对中性粒细胞或单核细胞的抗体。活动期SLE患者的血清能够抑制伴刀豆球蛋白A对正常血液淋巴细胞的激活，使其成为抑制细胞。后者通过共培养伴刀豆球蛋白A激活的细胞与自体淋巴细胞，然后用植物血凝素激活增殖反应或用美洲商陆有丝分裂原激活B细胞免疫球蛋白（IG）合成和分泌来测定。用吸附的活性SLE血清处理的抑制细胞与植物血凝素培养物的特异性掺入显示值为67+/-13（平均值+/-SD）。该值与用无活性SLE血清或正常血清池处理的细胞的值显着不同（P < 0.001）。在B细胞靶参数方面观察到类似的结果。对于用吸附的活性SLE血清处理的抑制细胞，在含有美洲商陆有丝分裂原的培养物上清液中的细胞质IG和IgG值分别为17+/-5%和717+/-134 ng/培养物。这与用非活性SLE血清或用正常血清池处理的那些显著不同。抗抑制细胞因子被证明是IgG，不依赖补体，无细胞毒性，在37 ℃和室温下有活性，但在4 ℃下无活性，并且可被T细胞吸附。活动性SLE患者血清中的抑制性T细胞抗体可能是活动性SLE中观察到的抑制性T细胞功能障碍的原因。抗抑制细胞抗体的诱导机制尚不清楚。
Circulating antibodies that could be responsible for the suppressor thymus-derived (T)-cell dysfunction in active systemic lupus erythematosus (SLE) were investigated. Sera from 14 active and inactive SLE patients were compared with a pool of 22 normal sera. All sera were adsorbed with a pool of normal platelets to exclude antihistocompatibility leukocyte antigen antibodies; with AB erythrocytes to exclude isohemagglutinins; and with a pool of normal bone marrow-derived (B) lymphocytes, monocytes, and neutrophils to deplete anti-B-cell antibodies, Fc-receptor antibodies, and antibodies directed against neutrophils or monocytes. Sera from active SLE patients were capable of inhibiting the activation of normal, blood lymphocytes by concanavalin A to become suppressor cells. The latter were assayed by coculturing the concanavalin A-activated cells with autologous lymphocytes, which were then activated with either phytohemagglutinin for proliferative response or with pokeweed mitogen for B-cell immunoglobulin (Ig) synthesis and secretion. Specific incorporation of cultures with phytohemagglutinin showed a value of 67+/-13 (mean+/-SD) for suppressor cells treated with adsorbed, active SLE sera. This value was significantly different (P < 0.001) from that of cells treated with the inactive SLE sera or with the pool of normal sera. Similar findings were seen with respect to the B-cell target parameters. Cytoplasmic Ig and IgG in supernates of cultures with pokeweed mitogen showed values of 17+/-5% and 717+/-134 ng/culture, respectively, for suppressor cells treated with the adsorbed, active SLE sera. This was significantly different from those treated with the inactive SLE sera or with the pool of normal sera. The antisuppressor-cell factor was shown to be IgG, complement independent, not cytotoxic, active at 37 degrees C and at room temperature, but not at 4 degrees C, and adsorbable with T cells. Suppressor T-cell antibody in sera of active SLE patients could be responsible for the observed suppressor T-cell dysfunction seen in active SLE. The mechanisms responsible for the induction of the antisuppressor-cell antibody are unknown.