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Inflammation-induced proteolytic processing of the SIRP? cytoplasmic ITIM in
neutrophils propagates a proinflammatory state
#MMPMID24026300
Zen K
; Guo Y
; Bian Z
; Lv Z
; Zhu D
; Ohnishi H
; Matozaki T
; Liu Y
Nat Commun
2013[]; 4
(?): 2436
PMID24026300
show ga
Signal regulatory protein ? (SIRP?), an immunoreceptor tyrosine-based inhibitory
motif (ITIM)-containing receptor, is an essential negative regulator of leukocyte
inflammatory responses. Here we report that SIRP? cytoplasmic signalling ITIMs in
neutrophils are cleaved during active inflammation and that the loss of SIRP?
ITIMs enhances the polymorphonuclear leukocyte (PMN) inflammatory response. Using
human leukocytes and two inflammatory models in mice, we show that the cleavage
of SIRP? ITIMs in PMNs but not monocytes occurs at the post-acute stage of
inflammation and correlates with increased PMN recruitment to inflammatory loci.
Enhanced transmigration of PMNs and PMN-associated tissue damage are confirmed in
mutant mice expressing SIRP? but lacking the ITIMs. Moreover, the loss of SIRP?
ITIMs in PMNs during colitis is blocked by an anti-interleukin-17 (IL-17)
antibody. These results demonstrate a SIRP?-based mechanism that dynamically
regulates PMN inflammatory responses by generating a CD47-binding but
non-signalling SIRP? 'decoy'.
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