SHIP is a hematopoietic‐specific lipid phosphatase that dephosphorylates PI3K‐generated PI(3,4,5)‐trisphosphate. SHIP removes this second messenger from the cell membrane blunting PI3K activity in immune cells. Thus, SHIP negatively regulates ma...
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https://www.riss.kr/link?id=O119685890
2018년
-
0741-5400
1938-3673
SCI;SCIE;SCOPUS
학술저널
1053-1064 [※수록면이 p5 이하이면, Review, Columns, Editor's Note, Abstract 등일 경우가 있습니다.]
0
상세조회0
다운로드다국어 초록 (Multilingual Abstract)
SHIP is a hematopoietic‐specific lipid phosphatase that dephosphorylates PI3K‐generated PI(3,4,5)‐trisphosphate. SHIP removes this second messenger from the cell membrane blunting PI3K activity in immune cells. Thus, SHIP negatively regulates ma...
SHIP is a hematopoietic‐specific lipid phosphatase that dephosphorylates PI3K‐generated PI(3,4,5)‐trisphosphate. SHIP removes this second messenger from the cell membrane blunting PI3K activity in immune cells. Thus, SHIP negatively regulates mast cell activation downstream of multiple receptors. SHIP has been referred to as the “gatekeeper” of mast cell degranulation as loss of SHIP dramatically increases degranulation or permits degranulation in response to normally inert stimuli. SHIP also negatively regulates Mϕ activation, including both pro‐inflammatory cytokine production downstream of pattern recognition receptors, and alternative Mϕ activation by the type II cytokines, IL‐4, and IL‐13. In the SHIP‐deficient (SHIP−/−) mouse, increased mast cell and Mϕ activation leads to spontaneous inflammatory pathology at mucosal sites, which is characterized by high levels of type II inflammatory cytokines. SHIP−/− mast cells and Mϕs have both been implicated in driving inflammation in the SHIP−/− mouse lung. SHIP−/− Mϕs drive Crohn's disease‐like intestinal inflammation and fibrosis, which is dependent on heightened responses to innate immune stimuli generating IL‐1, and IL‐4 inducing abundant arginase I. Both lung and gut pathology translate to human disease as low SHIP levels and activity have been associated with allergy and with Crohn's disease in people. In this review, we summarize seminal literature and recent advances that provide insight into SHIP's role in mast cells and Mϕs, the contribution of these cell types to pathology in the SHIP−/− mouse, and describe how these findings translate to human disease and potential therapies.
Review on SHIP's role in mast cell and macrophage activation in vitro, in the SHIP−/− mouse, and human immune‐mediated diseases.
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