Neutrophils Require SHP1 To Regulate IL-1 beta Production and Prevent Inflammatory Skin Disease
Details
Publication Year 2011-01-15,Volume 186,Issue #2,Page 1131-1139
Journal Title
JOURNAL OF IMMUNOLOGY
Publication Type
Journal Article
Abstract
The regulation of neutrophil recruitment, activation, and disposal is pivotal for circumscribed inflammation. SHP1(Y208N/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 SHP1(Y208N/Y208N) mice display increased pro-IL-1 beta production due to altered responses to MyD88-dependent and MyD88-independent signals. The IL-1R-dependent inflammatory disease in SHP1(Y208N/Y208N) mice develops independently of caspase 1 and proteinase 3 and neutrophil elastase. In response to Fas ligand, a caspase 1-independent inducer of IL-1 beta production, neutrophils from SHP1(Y208N/Y208N) mice produce elevated levels of IL-1 beta but display reduced caspase 3 and caspase 7 activation. In neutrophils deficient in SHP1, IL-1 beta induces high levels of pro-IL-1 beta suggesting the presence of a paracrine IL-1 beta loop. These data indicate that the neutrophil-and IL-1-dependent disease in SHP1(Y208N/Y208N) mice is a consequence of loss of negative regulation of TLR and IL-1R signaling. The Journal of Immunology, 2011, 186: 1131-1139.
Publisher
AMER ASSOC IMMUNOLOGISTS
Keywords
MOTH-EATEN MICE; NECROSIS-FACTOR-ALPHA; TYROSINE-PHOSPHATASE; GENE-EXPRESSION; RESPIRATORY BURST; INFLUENZA-VIRUS; CELL LYMPHOMA; DEATH DOMAIN; MUTANT MICE; NPM-ALK
Research Division(s)
Cancer And Haematology; Structural Biology; Immunology
Terms of Use/Rights Notice
Copyright © 2011 by The American Association of Immunologists, Inc.


Creation Date: 2011-01-15 12:00:00
Last Modified: 2014-12-23 12:06:25
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