Lymphocytes In Rheumatoid Arthritis Research Articles

MIF production of lymphocytes from patients with rheumatoid arthritis with antigen-antibody complexes.

Immune complexes, human erythrocytes coated with human IgG antibody, inhibit the migration of lymphocytes from rheumatoid arthritis (RA) patients. No correlation could be observed between migration inhibition and Waaler-Rose titre (sheep cell agglutination titre) in inidvidual patients. Production of migration inhibitory factor (MIF) could be detected in 16 of 20 cultures of RA lymphocytes incubated with antigen-antibody complexes, when the supernates were tested with guinea pig macrophages. Only two supernates of healthy persons showed migration inhibition activity under these conditions. The results suggest that migration inhibition by antigen antibody complexes in RA represents a true reaction of delayed hypersensitivity.

Rosette formation by peripheral blood lymphocytes in rheumatoid arthritis.

Rosette formation by peripheral blood lymphocytes in rheumatoid arthritis.

Studies of antilymphocyte antisera produced against normal and rheumatoid arthritis lymphocytes.

AbstractRabbit antisera were made against pooled normal human lymphocytes and against those from patients with active rheumatoid arthritis. Sera were subsequently absorbed to remove antibody to human erythrocytes and plasma proteins. Most antilymphocyte antisera showed considerable cytotoxic or complement fixing antibody after immunization, however a striking deficit (6 of 12 animals) in the activity of the antisera against RA lymphocytes was noted when blast transformation of lymphocytes was used as a test of antilymphocyte serum (ALS) antibody.

Altered reactivity in mixed lymphocyte culture of lymphocytes from patients with rheumatoid arthritis.

AbstractLymphocytes from patients with rheumatoid arthritis were studied in one‐way stimulation mixed leukocyte culture (MLC) and results compared with cultured pairs of rheumatoid and normal lymphocytes. In 14 of 22 experiments, no lymphocyte stimulation was noted when rheumatoid arthritis lymphocytes obtained from unrelated patients were studied in MLC. Normal lymphocytes produced stimulation of rheumatoid cells in 16 of 22 instances, and rheumatoid lymphocytes induced transformation of normal subjects' lymphocytes in 19 of 22 experiments. Marked alteration in mutual lymphocyte stimulation was thus recorded when cells from some patients with rheumatoid arthritis were studied together.