title: Impaired generation of high-affinity interleukin-2 receptors in the autologous mixed lymphocyte reaction in rheumatoid arthritis.
abstract: We examined the expression of high-affinity interleukin (IL)-2 receptors (IL-2R) as well as Tac and HLA-DR antigens on peripheral blood (PB) T cells from 11 rheumatoid arthritis (RA) patients and 8 healthy controls induced in the autologous mixed lymphocyte reaction (AMLR). The proportion of HLA-DR- and Tac-bearing T cells and expression of these activation antigens were higher in patients relative to controls (P less than 0.01) in freshly isolated unstimulated PB mononuclear cells. AMLR stimulation of RA T cells failed to induce an increase in the proportion of HLA-DR and Tac-bearing T cells which was observed in health controls. After AMLR stimulation the number of high-affinity IL-2R were significantly lower in RA patients compared with controls (P less than 0.01). The number of high-affinity IL-2R on patient T cells correlated strongly with AMLR reactivity as measured by [3H]thymidine incorporation (r = 0.821, P = 0.002). The results suggest that the AMLR defect in RA may result from impaired generation of high-affinity IL-2R.
authors.affiliation: Department of Medicine, Wellesley Hospital, University of Toronto, Ontario, Canada.
authors.forename: F
authors.initials: F
authors.lastname: Akasu
authors.forename: L
authors.initials: L
authors.lastname: Poplonski
authors.forename: K M
authors.initials: KM
authors.lastname: Snow
authors.forename: R
authors.initials: R
authors.lastname: Volpe
authors.forename: E C
authors.initials: EC
authors.lastname: Keystone
mesh_terms: D000328:Adult; D001172:Arthritis, Rheumatoid / Q000473:pathology*; D005260:Female; D005455:Fluorescent Antibody Technique; D006801:Humans; D007700:Kinetics; D008213:Lymphocyte Activation; D007959:Lymphocyte Culture Test, Mixed; D008875:Middle Aged; D015375:Receptors, Interleukin-2 / Q000502:physiology*; D013601:T-Lymphocytes / Q000276:immunology / Q000648:ultrastructure
chemical_list: D015375:Receptors, Interleukin-2