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The Journal of Immunology, 1999, 162: 1246-1251.
Copyright © 1999 by The American Association of Immunologists

IL-17 Is Produced by Some Proinflammatory Th1/Th0 Cells But Not by Th2 Cells1

Tanja Aarvak2,*, Martine Chabaud{dagger}, Pierre Miossec{dagger} and Jacob B. Natvig*

* Institute of Immunology, Laboratory of Rheumatology Research, The National Hospital, Oslo, Norway; and {dagger} Department of Immunology and Rheumatology, Hôpital Edourd Herriot and Immunovirology Laboratory UMR Centre National de la Recherche Scientifique 5537, Faculté de Médecine Laennec, Lyon, France

IL-17 is defined as a proinflammatory cytokine and produced by activated CD4+ T cells. In rheumatoid arthritis synovial tissue, high levels of IL-17 contribute to IL-6 production by synoviocytes. The present study was performed to see whether Th cells that produce IL-17 are associated with the Th1, Th2, or Th0 subset. Thirty-three CD4+, {alpha}ß+ T cell clones were developed from synovial membranes and synovial fluid of rheumatoid arthritis patients. Thirteen clones were defined as Th1 since they produced IFN-{gamma} but not IL-4, and four clones were defined as Th0 type that produced both IL-4 and IFN-{gamma}. Sixteen clones were defined as Th2 since they produced high levels of IL-4 and/or IL-10 but not IFN-{gamma}. IL-17 was measured in a bioassay, where IL-6 production from synoviocytes was a measurement for IL-17 activity in the presence and absence of blocking anti-IL-17 mAb. Three Th1 clones and two Th0 clones produced IL-17. In contrast, none of the sixteen Th2 clones analyzed produced IL-17. In addition, six Th2 clones were further cultured in conditions that induced a switch to Th1 type. Induction of this Th1 phenotype also led to production of IL-17 in two of these clones. The results demonstrate that some cells of the Th1/Th0 phenotype produce IL-17 but not cells of the Th2 phenotype. Thus, IL-17 may define a new subset of T cells, and IL-17 production appears to be a mechanism for Th1/Th0 cells, the most frequent Th subtype present in the rheumatoid synovium, to contribute to the local inflammatory reactions.




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