Impaired T-lymphocyte colony formation in lipoid nephrosis.
The T-colony-forming capacity was examined in 13 normal subjects and 14 patients with biopsy-proven lipoid nephrosis (LN). Eighteen additional patients with other well-defined forms of glomerulonephritis were studied as a disease control. Significantly fewer T lymphocyte colonies were found in LN patients and the nephrotic syndrome (NS) than in normal controls. A similar change could be observed in the groups with other types of NS. LN patients with NS had the lowest values of T-colony-forming cells (TCFC), but there was no statistically significant difference between the groups of nephrotic subjects. It was also of interest that peripheral blood lymphocytes (PBL) from 3 patients with lupus nephritis (SLE) produced significantly low levels of TCFC. The lower levels of TCFC in LN could be enhanced when exogenous interleukin 2 (IL 2) was added to the system. We also examined the production of T-colony-stimulating factor (TCSF). The TCSF production by stimulated 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.
D000293:Adolescent; D000328:Adult; D000368:Aged; D002648:Child; D005260:Female; D005921:Glomerulonephritis / Q000276:immunology; D006801:Humans; D007376:Interleukin-2 / Q000494:pharmacology; D008213:Lymphocyte Activation; D008297:Male; D008875:Middle Aged; D009402:Nephrosis, Lipoid / Q000276:immunology*; D010835:Phytohemagglutinins / Q000494:pharmacology; D013234:Stem Cells / Q000276:immunology; D013601:T-Lymphocytes / Q000187:drug effects / Q000276:immunology*
D007376:Interleukin-2; D010835:Phytohemagglutinins