Neutrophils require SHP1 to regulate IL-1β production and prevent inflammatory skin disease

BA Croker; RS Lewis; JJ Babon; JD Mintern; DE Jenne; D Metcalf; JG Zhang; LH Cengia; JA O'Donnell; AW Roberts

Journal article

Neutrophils require SHP1 to regulate IL-1β production and prevent inflammatory skin disease

BA Croker, RS Lewis, JJ Babon, JD Mintern, DE Jenne, D Metcalf, JG Zhang, LH Cengia, JA O'Donnell, AW Roberts

Journal of Immunology | AMER ASSOC IMMUNOLOGISTS | Published : 2011

DOI: 10.4049/jimmunol.1002702

Abstract

The regulation of neutrophil recruitment, activation, and disposal is pivotal for circumscribed inflammation. SHP1Y208N/Y208N mutant mice develop severe cutaneous inflammatory disease that is IL-1R dependent. Genetic reduction in neutrophil numbers and neutrophilic responses to infection is sufficient to prevent the spontaneous initiation of this disease. Neutrophils from SHP1Y208N/Y208N mice display increased pro-IL-1β production due to altered responses to MyD88-dependent and MyD88-independent signals. The IL-1R-dependent inflammatory disease in SHP1Y208N/Y208N mice develops independently of caspase 1 and proteinase 3 and neutrophil elastase. In response to Fas ligand, a caspase 1-independ..

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University of Melbourne Researchers

Jeffrey Babon Author

Justine Mintern Author

Andrew Roberts Author

Related Projects (2)

CAREER DEVELOPMENT AWARD - CDA LEVEL 1 BIOMEDICAL

Understanding the killing of virus infected cells.

Viruses provoke devastating disease. The immune system kills cells that are infected with viruses. To do this, immune cells release granules..

Grants

Awarded by National Health and Medical Research Council (NHMRC)

Awarded by Career Development award

Awarded by Australian Research Council QEII

Awarded by National Institutes of Health

Awarded by NHMRC Independent Research Institutes

Awarded by Australian Research Council

Funding Acknowledgements

B.A.C. was supported by a National Health and Medical Research Council (NHMRC) CJ Martin fellowship (356262), a Career Development award (575531), and an Australian Research Council QEII fellowship (DP1094854). J.D.M. was supported by a Career Development award (637374). A. W. R. was supported by an NHMRC Practitioner fellowship (356213) and a Victorian Cancer Agency fellowship. D. M. was supported by the Carden Fellowship of the Cancer Council of Victoria. Work performed at The Scripps Research Institute was supported by National Institutes of Health Contract HHSN272200700038C. Work performed at The Walter and Eliza Hall Institute of Medical Research was supported by NHMRC Grants 461219, 508905, and 637367, a Victorian State Government Operational Infrastructure Support grant, and the NHMRC Independent Research Institutes Infrastructure Support Scheme (361646).