Journal article

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

Takashi Ushiki, Nicholas D Huntington, Stefan P Glaser, Hiu Kiu, Angela Georgiou, Jian-Guo Zhang, Donald Metcalf, Nicos A Nicola, Andrew W Roberts, Warren S Alexander

PLOS ONE | PUBLIC LIBRARY SCIENCE | Published : 2016

Abstract

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 char..

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Grants

Awarded by Australian National Health and Medical Research Council (NHMRC)


Funding Acknowledgements

This work was supported by a Program Grant (1016647), Fellowships (WSA:1058344, NDH:0461276, NAN:1078737, AWR:637309, 1079560) and an Independent Research Institutes Infrastructure Support Scheme Grant (361646) from the Australian National Health and Medical Research Council (NHMRC, https://www.nhmrc.gov.au), a Victorian State Government Operational Infrastructure Support Grant and the Australia Cancer Research Fund (https://acrf.com.au). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.