1629 PRODUCTION OF THE LYMPHOKINE, SOLUBLE IMMUNE RESPONSE SUPPRESSOR (SIRS) BY PATIENTS WITH NEPHROTIC SYNDROME
1629 PRODUCTION OF THE LYMPHOKINE, SOLUBLE IMMUNE RESPONSE SUPPRESSOR (SIRS) BY PATIENTS WITH NEPHROTIC SYNDROME
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1629 肾病综合征患者生产淋巴因子、可溶性免疫反应抑制剂 (SIRS)
DOI：
10.1203/00006450-198504000-01653
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发表时间：
1985
影响因子：
3.6
通讯作者：
T. Aune
中科院分区：
文献类型：
--
作者：
H. Schnaper;T. Aune
肾病患者通常表现出原因不明的免疫反应抑制。在上一次SPR会议上，我们报道了活动期微小病变肾病综合征(MCNS)或膜增生性肾小球肾炎(MPGN)患者的尿中排泄SIRS。这种淋巴因子由干扰素或有丝分裂原激活的抑制性T细胞在体外产生，抑制正常细胞和肿瘤细胞的分裂以及B淋巴细胞的抗体分泌。SIRS活性在类固醇治疗开始后但肾病缓解前从尿中消失。为了确定血清SIRS水平升高是否也与这些疾病有关，我们检测了4例患者(3MCNS，1MPGN)的SIRS活性。在培养终浓度为2-10%时，患者血清对商陆丝裂原激活的淋巴细胞产生免疫球蛋白的抑制率为55-70%，而非对照血清；抑制活性可被抗SIRS抗体从血清中吸收。从两例患者(1MCNS，1MPGN)获得的淋巴细胞产生SIRS，而不需要外源性物质激活。这些数据表明，肾病伴MCNS或MPGN患者的淋巴细胞持续产生SIRS。这可能是血清和尿液中SIRS水平升高的原因，也可能是这些患者免疫抑制的原因。最后，氢化可的松(10−6~10−7M)抑制激活的淋巴细胞产生SIRS，这可能是类固醇治疗后SIRS停止排泄的原因。
Nephrotic patients often show suppressed immune responsiveness of unknown origin. At the last SPR meeting we reported that patients with active minimal change nephrotic syndrome (MCNS) or membranoproliferative glomerulonephritis (MPGN) excrete SIRS in their urine. This lymphokine, produced in vitro by interferon- or mitogen-activated suppressor T cells, inhibits division by normal and neoplastic cells and antibody secretion by B lymphocytes. SIRS activity disappears from urine after initiation of steroid therapy but before remission of nephrosis. To determine whether increased serum SIRS levels are also associated with these diseases, sera from four patients (3MCNS, 1MPGN) were assayed for SIRS activity. Patient sera, but not control sera, suppressed immunoglobulin production by pokeweed mitogen-activated lymphocytes by 55–70% at a final concentration of 2-10% in culture; suppressive activity was absorbed from serum by monoclonal anti-SIRS antibody. Lymphocytes obtained from two patients (1MCNS, 1MPGN) produced SIRS without requiring activation by exogenous agents. These data suggest that lymphocytes of nephrotic patients with MCNS or MPGN are continuously producing SIRS. This may account for the increased levels of SIRS in sera and urine and may also account for immunosuppression in these patients. Finally, hydrocortisone (10−6 to 10−7M) inhibited production of SIRS by activated lymphocytes; this may explain cessation of SIRS excretion after initiation of steroid therapy.