Matsumoto K, Okano K, Yoshizawa N, Hatano M
Second Department of Internal Medicine, Nihon University School of Medicine, Tokyo, Japan.
Int Arch Allergy Appl Immunol. 1988;85(1):94-8. doi: 10.1159/000234480.
The T-colony-forming capacity was examined in 13 normal subjects and 8 patients with biopsy-proven focal glomerular sclerosis (FGS). Fifteen patients with chronic mesangial proliferative glomerulonephritis (CGN) without renal insufficiency were studied as a disease control. The two main assays used were the counting of T colonies formed by the patients' lymphocytes, and the measurement of T-colony-forming activity in conditioned medium from cultures of patients' lymphocytes. The levels of T-colony-forming cells (TCFC) and T-colony-stimulating factor (TCSF) were decreased in patients with FGS compared with those in normal controls and lower in FGS patients with the nephrotic syndrome (NS) than in those without NS. In contrast, these parameters in CGN patients with or without NS did not differ from normal subjects. TCSF activity for TCFC in both normal individuals and FGS patients was removed from media conditioned by phytohemagglutinin (PHA)-stimulated peripheral blood lymphocytes (PHA-LCM) with interleukin-2 (IL-2) receptor bearing cultured T cells. These in vitro findings suggest that IL-2 is the essential factor contained in PHA-LCM. Thus, depressed TCFC in FGS patients with NS may result in part from impaired generation of TCSF by lymphocytes.
对13名正常受试者和8名经活检证实为局灶性肾小球硬化(FGS)的患者进行了T集落形成能力检测。将15例无肾功能不全的慢性系膜增生性肾小球肾炎(CGN)患者作为疾病对照进行研究。所使用的两种主要检测方法是对患者淋巴细胞形成的T集落进行计数,以及测量患者淋巴细胞培养条件培养基中的T集落形成活性。与正常对照组相比,FGS患者的T集落形成细胞(TCFC)和T集落刺激因子(TCSF)水平降低,且肾病综合征(NS)的FGS患者低于无NS的患者。相比之下,有或无NS的CGN患者的这些参数与正常受试者无差异。用携带白细胞介素-2(IL-2)受体的培养T细胞从植物血凝素(PHA)刺激的外周血淋巴细胞(PHA-LCM)条件培养基中去除正常个体和FGS患者中TCFC的TCSF活性。这些体外研究结果表明,IL-2是PHA-LCM中所含的关键因子。因此,NS的FGS患者中TCFC降低可能部分是由于淋巴细胞产生TCSF受损所致。