Rapid inflammation in mice lacking both SOCS1 and SOCS3 in hematopoietic cells
- Author(s)
- Ushiki, T; Huntington, ND; Glaser, SP; Kiu, H; Georgiou, A; Zhang, JG; Metcalf, D; Nicola, NA; Roberts, AW; Alexander, WS;
- Details
- Publication Year 2016,Volume 11,Issue #9,Page e0162111
- Journal Title
- PLoS One
- Publication Type
- Journal Article
- 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 IFNgamma and gamma-common (gammac) 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.
- Publisher
- PLOS
- Research Division(s)
- Cancer And Haematology; Molecular Immunology
- PubMed ID
- 27583437
- Publisher's Version
- https://doi.org/10.1371/journal.pone.0162111
- Open Access at Publisher's Site
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0162111- NHMRC Grants
- NHMRC/1016647, NHMRC/1058344, NHMRC/1078737, NHMRC/637309, NHMRC/1079560,
- Terms of Use/Rights Notice
- Refer to copyright notice on published article.
Creation Date: 2016-10-03 03:38:09
Last Modified: 2016-10-03 04:50:14