Origin of defective T lymphocyte-suppressor activating factor interaction in patients with rheumatoid arthritis.
We previously examined the generation of T cell released suppressor activity (TRSA) from peripheral blood T cells from patients with rheumatoid arthritis (RA) in response to a soluble suppressor activating factor (SAF) produced by a 6-thioguanine resistant mutant of the human T cell line CEM. We reported (Lau et al., 1985 Clin. exp. Immunol. 61, 481) that T cells from a substantial proportion of RA patients exhibited impaired TRSA release. To delineate further the TRSA abnormality observed in patients with active RA, we evaluated the kinetics of SAF activation, precursor frequency of SAF reactive cells and quantity of activated SAF released on a per cell basis. The results showed that a lower precursor frequency of SAF reactive cells accounted for defective TRSA release in a majority of RA patients, while TRSA release on a per cell basis was normal. The defective TRSA response to SAF could not be explained by abnormal dose kinetics of SAF, time kinetics of TRSA release or prior in vivo lymphocyte activation of the RA T cells.
D000328:Adult; D000368:Aged; D001172:Arthritis, Rheumatoid / Q000276:immunology*; D002452:Cell Count; D002454:Cell Differentiation; D005260:Female; D006801:Humans; D007700:Kinetics; D008297:Male; D008875:Middle Aged; D013491:Suppressor Factors, Immunologic / Q000096:biosynthesis*; D050378:T-Lymphocytes, Regulatory / Q000276:immunology* / Q000473:pathology
D013491:Suppressor Factors, Immunologic