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Koichi Matsumoto, MD, Department of Nephrology, Prince Henry’s Hospital, St. Kilda Road, Melbourne 3004, (Australia) Dear Sir, Several lines of evidence indicate that cell-mediated immunity (CMI) is impaired in patients with lipoid nephrosis (LN) [8]. We have recently shown that LN patients with the nephrotic syndrome (NS) have a systemic disorder of CMI, characterized by decreased T cell numbers, depressed delayed hypersensitivity reactions and impaired local graft-versus-host reactions [1, 4–6]. Our previous studies [2,3] also illustrated an increase in concana-valin A-induced suppressor cell activity in the majority of LN patients in relapse. In the present study a more reliable method – T lymphocyte colony assay – was used to study CMI in 14 patients with LN and 13 normal individuals. Colony-forming assays were performed by a one-step culture method with some modifications [9]. The number of T colony-forming cells (TCFC) in the mononuclear cell preparation of LN patients and the NS was found to be significantly lower than in normal subjects, while LN in remission had mean values of the TCFC capacity not significantly different in respect to normal controls. We also examined the activity of T colony-stimulating factor (TCSF) in media conditioned by 0.25% phytohemagglut-inin (PHA-P) stimulated peripheral blood lymphocytes (PHA-LCM). The TCSF activity by stimulated peripheral blood lymphocytes (PBL) from LN patients was lower than in normal subjects. To explain our observations, we presumed that the T colony dysfunction seen in LN patients with NS might in part be due to the decreased TCSF activity. To further demonstrate the role of interleukin 2 (IL 2) in T colony formation, we used a biological assay to remove specifically IL 2 from PHA-LCM. PHA-LCM was absorbed for 1 h × 3 at 37 ¤C using 108 IL 2-dependent cultured T cells/ml according to the method of Rey et al. [7]. Prior to absorption, cells were incubated for 24 h without IL 2 in order to remove bound IL 2. Absorbed 100 9070 60 50 1⁄8o 5 30 20-

Evaluation of T Colony-Stimulating Factor in Patients with Lipoid Nephrosis