2004
DOI: 10.1016/j.immuni.2004.07.010
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Abstract: An initial exposure to lipopolysaccharide (LPS) induces a transient state of hyporesponsiveness to a subsequent challenge with LPS. The mechanism underlying this phenomenon, termed endotoxin tolerance, remains poorly understood despite a recent resurgence of interest in this area. We demonstrate herein that SHIP(-/-) bone marrow-derived macrophages (BMmphis) and mast cells (BMMCs) do not display endotoxin tolerance. Moreover, an initial LPS treatment of wild-type BMmphis or BMMCs increases the level of SHIP, b… Show more

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Cited by 279 publications
(309 citation statements)
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“…SHIP-1 is a hematopoietic-specific 59 inositol phosphatase that represses the antiapoptotic and proinflammatory PI3K pathway (20,26), which is of particular importance in MFs. M2 AMF polarization was first identified in SHIP-1 2/2 mice that spontaneously developed lung disease (8), making SHIP-1 2/2 mice an invaluable model for examining MF-mediated mechanisms underlying chronic lung disease.…”
Section: Identification Of Amf Subpopulations In Chronic Lung Diseasementioning
confidence: 99%
“…SHIP-1 is a hematopoietic-specific 59 inositol phosphatase that represses the antiapoptotic and proinflammatory PI3K pathway (20,26), which is of particular importance in MFs. M2 AMF polarization was first identified in SHIP-1 2/2 mice that spontaneously developed lung disease (8), making SHIP-1 2/2 mice an invaluable model for examining MF-mediated mechanisms underlying chronic lung disease.…”
Section: Identification Of Amf Subpopulations In Chronic Lung Diseasementioning
confidence: 99%
“…67,68 Paradoxically, in a series of reports from another group, SHIP1 blocked Tnf and Il6 secretion upon TLR3 or TLR4 stimulation, but induced Il12 and expression of surface co-stimulatory molecules upon TLR stimulation, suggesting a more complex role for SHIP1 in downstream TLR signaling. [69][70][71][72] Consequently, SHIP1-deficient DCs were functionally incompetent for priming Th1 effector T cells. 69,70 These conflicting reports warrant further and more detailed investigation into the molecular mechanism of SHIP1-mediated control of the TLR pathway.…”
Section: Pathways Of Activation By Toll-like Receptorsmentioning
confidence: 99%
“…In addition to IRAK-M, many negative regulators of TLR signaling have been identified, including the TLR homolog RP105, Src homology 2-containing inositol-5ā€²-phosphatase (SHIP), short form of MyD88, ST2, SIGIRR, Triad3A, A20, and SOCS-1 (44)(45)(46)(47)(48)(49)(50)(51)(52). Many of these molecules have been implicated in the development of endotoxin tolerance.…”
Section: Figurementioning
confidence: 99%