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Journal: Immunology and cell biology
Languages: English
Types: Article
Subjects: IL-1β, Suppressor of Cytokine Signaling-3, IL-6, Article, SOCS3

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mesheuropmc: digestive, oral, and skin physiology
The lack of expression of the Suppressor of Cytokine Signalling-3 (SOCS3) or inactivation of the negative regulatory capacity of SOCS3 has been well documented in rheumatoid arthritis, viral hepatitis and cancer. The specific qualitative and quantitative consequences of SOCS3-deficiency on IL-6-mediated pro- and anti-inflammatory responses remain controversial in vitro and unknown in vivo. Mice with a conditional deletion of SOCS3 in hematopoietic cells develop lethal inflammatory disease during adult life and develop gross histopathological changes during experimental arthritis, typified by elevated IL-6 levels. To clarify the nature of the IL-6 responses in vivo, we generated mice deficient in SOCS3 (SOCS3 −/Δ vav ) or both SOCS3 and IL-6 (IL-6 − / − /SOCS3 −/Δ vav ) and examined responses in models of acute and chronic inflammation. Acute responses to IL-1β were lethal to SOCS3 −/Δ vav mice but not IL-6 − / − /SOCS3 −/Δ vav mice, indicating that IL-6 was required for the lethal inflammation induced by IL-1β. Administration of IL-1β to SOCS3 −/Δ vav mice induced systemic apoptosis of lymphocytes in the thymus, spleen and lymph nodes that was dependent on the presence of IL-6. IL-6-deficiency prolonged survival of SOCS3 −/Δ vav mice and ameliorated spontaneous inflammatory disease developing during adult life. Infection of SOCS3 −/Δ vav mice with LCMV induced a lethal inflammatory response that was dependent on IL-6, despite SOCS3 −/Δ vav mice controlling viral replication. We conclude that SOCS3 is required for survival during inflammatory responses and is a critical regulator of IL-6 in vivo.

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