[Immunsuppressive factors in sera and synovial fluids of patients with rheumatoid arthritis (author's transl)]. 1979

A Lohrmann, and P A Berg, and S Goethe, and G König

Serum inhibitory factors (SIF) have been demonstrated in several infectious diseases and autoimmune disorders. Most likely, they are caused by an immune reaction, and their persistence indicates a chronic course. Sera and synovial fluids of 31 patients with rheumatoid arthritis and of 33 patients with arthrosis were therefore studied, in order to determine whether immunosuppressive factors exist only in inflammatory diseases and whether their titers correlate with the activity of the disease. PHA-induced stimulation of normal peripheral blood lymphocytes, measured as 3H thymidine uptake, in the presence of patients' serum, was related to lymphocyte stimulation observed in the presence of control sera. Using the MIF-agarose assay, the effect of sera and synovial fluids on the tuberculin-induced migration inhibition was also studied. Sera of 27 of 31 patients with rheumatoid arthritis inhibited mitogen-induced normal lymphocyte thymidine uptake and abolsihed migration inhibition, probably by blocking MIF-production. High titers appeared to predict an unfavourable course. In contrast, sera of all 33 patients with degenerative joint disease failed to exert these effects. Synovial fluids of all patients, irrespective of the nature of the underlying joint disease, did not affect lymphocyte stimulation or leukocyte migration. Other factors, such as immune complexes, cytotoxic antibodies, or drug metabolites could be excluded as potential causes of the observed effects exerted by rheumatoid arthritis sera. These results indicate that the presence of serum factors inhibiting PHA-induced lymphocyte stimulation and leukocyte migration inhibition, respectively, may be used as a diagnostic tool in the differential diagnosis of rheumatoid arthritis.

UI MeSH Term Description Entries
D007165 Immunosuppression Therapy Deliberate prevention or diminution of the host's immune response. It may be nonspecific as in the administration of immunosuppressive agents (drugs or radiation) or by lymphocyte depletion or may be specific as in desensitization or the simultaneous administration of antigen and immunosuppressive drugs. Antirejection Therapy,Immunosuppression,Immunosuppressive Therapy,Anti-Rejection Therapy,Therapy, Anti-Rejection,Therapy, Antirejection,Anti Rejection Therapy,Anti-Rejection Therapies,Antirejection Therapies,Immunosuppression Therapies,Immunosuppressions,Immunosuppressive Therapies,Therapies, Immunosuppression,Therapies, Immunosuppressive,Therapy, Immunosuppression,Therapy, Immunosuppressive
D008213 Lymphocyte Activation Morphologic alteration of small B LYMPHOCYTES or T LYMPHOCYTES in culture into large blast-like cells able to synthesize DNA and RNA and to divide mitotically. It is induced by INTERLEUKINS; MITOGENS such as PHYTOHEMAGGLUTININS, and by specific ANTIGENS. It may also occur in vivo as in GRAFT REJECTION. Blast Transformation,Blastogenesis,Lymphoblast Transformation,Lymphocyte Stimulation,Lymphocyte Transformation,Transformation, Blast,Transformation, Lymphoblast,Transformation, Lymphocyte,Activation, Lymphocyte,Stimulation, Lymphocyte
D008934 Mitogens Substances that stimulate mitosis and lymphocyte transformation. They include not only substances associated with LECTINS, but also substances from streptococci (associated with streptolysin S) and from strains of alpha-toxin-producing staphylococci. (Stedman, 25th ed) Mitogen,Phytomitogen,Phytomitogens
D002464 Cell Migration Inhibition Phenomenon of cell-mediated immunity measured by in vitro inhibition of the migration or phagocytosis of antigen-stimulated LEUKOCYTES or MACROPHAGES. Specific CELL MIGRATION ASSAYS have been developed to estimate levels of migration inhibitory factors, immune reactivity against tumor-associated antigens, and immunosuppressive effects of infectious microorganisms. Chemotaxis Inhibition,Chemotaxis Inhibitions,Inhibition, Chemotaxis,Inhibitions, Chemotaxis
D006801 Humans Members of the species Homo sapiens. Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man
D001172 Arthritis, Rheumatoid A chronic systemic disease, primarily of the joints, marked by inflammatory changes in the synovial membranes and articular structures, widespread fibrinoid degeneration of the collagen fibers in mesenchymal tissues, and by atrophy and rarefaction of bony structures. Etiology is unknown, but autoimmune mechanisms have been implicated. Rheumatoid Arthritis
D013582 Synovial Fluid The clear, viscous fluid secreted by the SYNOVIAL MEMBRANE. It contains mucin, albumin, fat, and mineral salts and serves to lubricate joints. Synovia,Fluid, Synovial,Fluids, Synovial,Synovial Fluids
D014373 Tuberculin A protein extracted from boiled culture of tubercle bacilli (MYCOBACTERIUM TUBERCULOSIS). It is used in the tuberculin skin test (TUBERCULIN TEST) for the diagnosis of tuberculosis infection in asymptomatic persons. PPD,PPD-B,PPD-CG,PPD-F,PPD-L,PPD-S,Purified Protein Derivative of Tuberculin,PPD B,PPD CG,PPD F,PPD L

Related Publications

A Lohrmann, and P A Berg, and S Goethe, and G König
November 1974, Annals of the rheumatic diseases,
A Lohrmann, and P A Berg, and S Goethe, and G König
December 1998, The Journal of rheumatology,
A Lohrmann, and P A Berg, and S Goethe, and G König
August 1975, The Journal of clinical investigation,
A Lohrmann, and P A Berg, and S Goethe, and G König
March 1975, Casopis lekaru ceskych,
A Lohrmann, and P A Berg, and S Goethe, and G König
February 1983, Arthritis and rheumatism,
A Lohrmann, and P A Berg, and S Goethe, and G König
February 1985, Clinical and experimental immunology,
A Lohrmann, and P A Berg, and S Goethe, and G König
October 1979, Ryumachi. [Rheumatism],
A Lohrmann, and P A Berg, and S Goethe, and G König
July 1988, Arthritis and rheumatism,
A Lohrmann, and P A Berg, and S Goethe, and G König
May 1992, The Journal of rheumatology,
Copied contents to your clipboard!