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Rapid Inflammation in Mice Lacking Both SOCS1 and SOCS3 in Hematopoietic Cells.
Ushiki, Takashi; Huntington, Nicholas D; Glaser, Stefan P; Kiu, Hiu; Georgiou, Angela; Zhang, Jian-Guo; Metcalf, Donald; Nicola, Nicos A; Roberts, Andrew W; Alexander, Warren S.
Afiliación
  • Ushiki T; Cancer and Haematology Division, The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia.
  • Huntington ND; Division of Transfusion and Regenerative Medicine, Niigata University Medical and Dental Hospital, Niigata, Japan.
  • Glaser SP; Molecular Immunology Division, The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia.
  • Kiu H; Department of Medical Biology, The University of Melbourne, Parkville, Victoria, Australia.
  • Georgiou A; Cancer and Haematology Division, The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia.
  • Zhang JG; Department of Medical Biology, The University of Melbourne, Parkville, Victoria, Australia.
  • Metcalf D; Cancer and Haematology Division, The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia.
  • Nicola NA; Cancer and Haematology Division, The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia.
  • Roberts AW; Cancer and Haematology Division, The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia.
  • Alexander WS; Department of Medical Biology, The University of Melbourne, Parkville, Victoria, Australia.
PLoS One ; 11(9): e0162111, 2016.
Article en En | MEDLINE | ID: mdl-27583437
The Suppressors of Cytokine Signalling (SOCS) proteins are negative regulators of cytokine signalling required to prevent excess cellular responses. SOCS1 and SOCS3 are essential to prevent inflammatory disease, SOCS1 by attenuating responses to IFNγ and gamma-common (γc) cytokines, and SOCS3 via regulation of G-CSF and IL-6 signalling. SOCS1 and SOCS3 show significant sequence homology and are the only SOCS proteins to possess a KIR domain. The possibility of overlapping or redundant functions was investigated in inflammatory disease via generation of mice lacking both SOCS1 and SOCS3 in hematopoietic cells. Loss of SOCS3 significantly accelerated the pathology and inflammatory disease characteristic of SOCS1 deficiency. We propose a model in which SOCS1 and SOCS3 operate independently to control specific cytokine responses and together modulate the proliferation and activation of lymphoid and myeloid cells to prevent rapid inflammatory disease.
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Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Células de la Médula Ósea / Proteína 1 Supresora de la Señalización de Citocinas / Proteína 3 Supresora de la Señalización de Citocinas / Inflamación Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Revista: PLoS One Asunto de la revista: CIENCIA / MEDICINA Año: 2016 Tipo del documento: Article País de afiliación: Australia

Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Células de la Médula Ósea / Proteína 1 Supresora de la Señalización de Citocinas / Proteína 3 Supresora de la Señalización de Citocinas / Inflamación Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Revista: PLoS One Asunto de la revista: CIENCIA / MEDICINA Año: 2016 Tipo del documento: Article País de afiliación: Australia