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    Online Resource
    Online Resource
    The American Association of Immunologists ; 2012
    In:  The Journal of Immunology Vol. 188, No. 1_Supplement ( 2012-05-01), p. 123.22-123.22
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 188, No. 1_Supplement ( 2012-05-01), p. 123.22-123.22
    Abstract: Objective: We investigated whether the OSM was induced SOCS3 in Treg and Th17 generation in type II collagen induced arthritis (CIA) mice. Method: Isolated T cell of CIA mice was incubated with Th17 or Treg differentiation condition for 30min or 3day. The Th17 and Treg culture condition was incubated with or without OSM 5, 10, 20 and 50 ng/ml. The cell lysated was analyzed using western blot for phospho(p)-STAT3705, p-STAT3727 andp-STAT5 IL-17production was measured in 3day culture supernatant. IL-17 and SOCS3 mRNA levels were analysis by real-time PCR. Result: OSM was increased p-STAT3705 in Th17 and Treg culture condition, but not p-STAT5. However, production of IL-17 and IL-17 mRNA was decreased in Th17 and Treg culture condition. Inaddition, the OSM was increased SOCS3 mRNA in Th17 and Treg condition. Next we investigated expression of OSM and SOCS3 mRNA levels in Treg cell. P-STAT5, OSM and SOCS3 were activated inTreg, while p-STAT3 was decreased. Although OSM was induced activation of STAT3, that was suppressed differentiation from Treg to Th17. These result ssuggest that OSM was regulated expression of SOCS3, thereby tightly regulated plastically differentiation of Treg and Th17. Conclusion: SOCS3 induced by OSM is an acting negative feedback loop and since OSM-mediated signaling is suppression IL-17 production in mouse CD4 T cells, which is provide for feedback inhibition of inflammatory response in the CIA.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    RVK:
    RVK:
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2012
    detail.hit.zdb_id: 1475085-5
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