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Research Article Free access | 10.1172/JCI110092
Division of Tumor Immunology, Sidney Farber Cancer Institute, Boston, Massachusetts 02115
Division of Immunology, The Children's Hospital Medical Center, Boston, Massachusetts 02115
Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115
Department of Pediatrics, Harvard Medical School, Boston, Massachusetts 02115
Arthritis Branch, National Institute of Arthritis, Metabolism, and Digestive Disease, Bethesda, Maryland 20205
Find articles by Morimoto, C. in: JCI | PubMed | Google Scholar
Division of Tumor Immunology, Sidney Farber Cancer Institute, Boston, Massachusetts 02115
Division of Immunology, The Children's Hospital Medical Center, Boston, Massachusetts 02115
Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115
Department of Pediatrics, Harvard Medical School, Boston, Massachusetts 02115
Arthritis Branch, National Institute of Arthritis, Metabolism, and Digestive Disease, Bethesda, Maryland 20205
Find articles by Reinherz, E. in: JCI | PubMed | Google Scholar
Division of Tumor Immunology, Sidney Farber Cancer Institute, Boston, Massachusetts 02115
Division of Immunology, The Children's Hospital Medical Center, Boston, Massachusetts 02115
Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115
Department of Pediatrics, Harvard Medical School, Boston, Massachusetts 02115
Arthritis Branch, National Institute of Arthritis, Metabolism, and Digestive Disease, Bethesda, Maryland 20205
Find articles by Borel, Y. in: JCI | PubMed | Google Scholar
Division of Tumor Immunology, Sidney Farber Cancer Institute, Boston, Massachusetts 02115
Division of Immunology, The Children's Hospital Medical Center, Boston, Massachusetts 02115
Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115
Department of Pediatrics, Harvard Medical School, Boston, Massachusetts 02115
Arthritis Branch, National Institute of Arthritis, Metabolism, and Digestive Disease, Bethesda, Maryland 20205
Find articles by Mantzouranis, E. in: JCI | PubMed | Google Scholar
Division of Tumor Immunology, Sidney Farber Cancer Institute, Boston, Massachusetts 02115
Division of Immunology, The Children's Hospital Medical Center, Boston, Massachusetts 02115
Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115
Department of Pediatrics, Harvard Medical School, Boston, Massachusetts 02115
Arthritis Branch, National Institute of Arthritis, Metabolism, and Digestive Disease, Bethesda, Maryland 20205
Find articles by Steinberg, A. in: JCI | PubMed | Google Scholar
Division of Tumor Immunology, Sidney Farber Cancer Institute, Boston, Massachusetts 02115
Division of Immunology, The Children's Hospital Medical Center, Boston, Massachusetts 02115
Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115
Department of Pediatrics, Harvard Medical School, Boston, Massachusetts 02115
Arthritis Branch, National Institute of Arthritis, Metabolism, and Digestive Disease, Bethesda, Maryland 20205
Find articles by Schlossman, S. in: JCI | PubMed | Google Scholar
Published March 1, 1981 - More info
The human inducer (T4+) and reciprocal cytotoxic/suppressor (T5+/T8+) subsets have been defined by monoclonal antibodies. In the present study, we examined the relationship of naturally occurring anti-T cell autoantibodies found in patients with active juvenile rheumatoid arthritis (JRA) to these subsets. In one approach, normal T cells were treated with anti-T4 or anti-T8 to eliminate the corresponding subset of cells and then analyzed for reactivity with JRA sera. It was found that JRA sera were reactive with only 15% of an enriched cytotoxic/suppressor population, whereas they reacted with 37% of an enriched inducer population. In reciprocal studies, JRA+ T cells were eliminated with JRA sera and complement and the residual T cells (JRA−) reacted with monoclonal antibodies and indirect immunofluorescence on a fluorescence-activated cell sorter. As expected, the JRA sera and complement treatment of unfractionated T cells markedly diminished the T4+ subset, whereas there was a concomitant increase in T cells reactive with anti-T5 and anti-T8. A similar diminution in T4+ T cells was found in the circulating peripheral T cell compartment of patients with active JRA who possessed the JRA antibody.
Functional studies demonstrated that removal of the JRA+ population of T cells diminished phytohemagglutinin and soluble antigen proliferative responses, both of which were previously shown to be functions of T4+ T cells. More importantly, in the absence of JRA+ T cells, pokeweed mitogen-stimulated immunoglobulin production was markedly enhanced, despite the concomitant increase in T5+/T8+ cytotoxic/suppressor cells. These results suggest that the JRA serum may define a Qal-like antigen found predominantly on the human inducer population which could activate suppressor and/or other feedback regulatory cells.