Rapid Inflammation in Mice Lacking Both SOCS1 and SOCS3 in Hematopoietic Cells

Download
Author
Ushiki, T; Huntington, ND; Glaser, SP; Kiu, H; Georgiou, A; Zhang, J-G; Metcalf, D; Nicola, NA; Roberts, AW; Alexander, WSDate
2016-09-01Source Title
PLoS OnePublisher
PUBLIC LIBRARY SCIENCEUniversity of Melbourne Author/s
Huntington, Nicholas; Alexander, Warren; Zhang, Jian-Guo; Glaser, Stephan; Nicola, Nicos; Roberts, AndrewAffiliation
Medical Biology (W.E.H.I.)Centre for Cancer Research
Metadata
Show full item recordDocument Type
Journal ArticleCitations
Ushiki, T., Huntington, N. D., Glaser, S. P., Kiu, H., Georgiou, A., Zhang, J. -G., Metcalf, D., Nicola, N. A., Roberts, A. W. & Alexander, W. S. (2016). Rapid Inflammation in Mice Lacking Both SOCS1 and SOCS3 in Hematopoietic Cells. PLOS ONE, 11 (9), https://doi.org/10.1371/journal.pone.0162111.Access Status
Open AccessAbstract
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.
Export Reference in RIS Format
Endnote
- Click on "Export Reference in RIS Format" and choose "open with... Endnote".
Refworks
- Click on "Export Reference in RIS Format". Login to Refworks, go to References => Import References