Proteoglycan‐induced polyarthritis and spondylitis adoptively transferred to naive (nonimmunized) BALB/c mice
- 1 June 1990
- journal article
- research article
- Published by Wiley in Arthritis & Rheumatism
- Vol. 33 (6) , 866-876
- https://doi.org/10.1002/art.1780330614
Abstract
Mononuclear cells from BALB/c mice with progressive polyarthritis and spondylitis induced by injection of fetal human articular cartilage proteoglycan (PG) were used to transfer arthritis by intravenous injection into irradiated, nonimmunized syngeneic mice. Successful transfer of arthritis to BALB/c mice required the injection of lymphocytes from mice with arthritis, along with 50 m̈g of human fetal PG, or lymphocytes stimulated in vitro with either fetal human PG or with mouse cartilage PG. In addition, interleukin‐2 or immune sera from animals with arthritis significantly reduced the time to onset of transferred disease. The onset of adoptively transferred arthritis, using cells and antigen, from the time of the first injection (38.2 ± 18.2 days, mean ± SD) was shortened if lymphocytes from mice with transferred arthritis were reinjected (retransferred) into other, irradiated syngeneic mice (6.1 ± 2.6 days). The appearance of autoreactive antibodies to mouse cartilage PG in the sera of mice with adoptively transferred arthritis (secondary or tertiary) preceded the appearance of the first clinical symptoms by a few days. The transfer of arthritis was blocked by pretreatment of donor (arthritic) lymphocytes with either anti‐T cell or anti‐B cell antibodies and complement. Exposure of mononuclear cells from mice with arthritis to PG, and its removal prior to transfer, also resulted in transfer of the arthritis. PG‐induced arthritis was not transferred to nonirradiated mice, nor to irradiated mice injected with lymphocytes from animals with primary arthritis without chondroitinase ABC‐digested fetal human PG. Arthritis never developed after injection of immune sera from mice with arthritis (without cells), nor when cells of nonarthritic animals were used with chondroitinase ABC‐digested fetal human PG, with or without interleukin‐2.This publication has 29 references indexed in Scilit:
- Cartilage proteoglycans as potential autoantigens in humans and in experimental animalsInflammation Research, 1988
- Evidence that a humoral immune response to autologous cartilage proteoglycan can participate in the induction of cartilage pathologyArthritis & Rheumatism, 1988
- T Lymphocytes in Collagen II‐Induced Arthritis in MiceScandinavian Journal of Immunology, 1985
- Passive transfer of collagen arthritis: Studies with affinity-purified anticollagen IgG prepared in rabbitsClinical Immunology and Immunopathology, 1984
- Connective tissue antigens stimulate collagenase production in arthritic diseasesCellular Immunology, 1984
- Type II collagen-induced arthritis in rats. Passive transfer with serum and evidence that IgG anticollagen antibodies can cause arthritis.The Journal of Experimental Medicine, 1982
- Immunisation against heterologous type II collagen induces arthritis in miceNature, 1980
- Antibodies to Type II Collagen in Relapsing PolychondritisNew England Journal of Medicine, 1978
- Cellular Sensitivity to Collagen in Rheumatoid ArthritisNew England Journal of Medicine, 1978
- Autoimmunity to type II collagen an experimental model of arthritis.The Journal of Experimental Medicine, 1977