Activation of Innate Immune Functions Sepsis by Controlling C 5 a-Mediated Pathway Exerts Protective Effects during The Phosphatidylinositol 3-Kinase Signaling

[1]  R. Schmidt,et al.  Cell-derived anaphylatoxins as key mediators of antibody-dependent type II autoimmunity in mice. , 2006, The Journal of clinical investigation.

[2]  M. Hallett,et al.  Localised PtdIns(3,4,5)P3 or PtdIns(3,4)P2 at the phagocytic cup is required for both phagosome closure and Ca2+ signalling in HL60 neutrophils , 2006, Journal of Cell Science.

[3]  E. Ong,et al.  Role of phosphatidylinositol 3-kinase-γ in mediating lung neutrophil sequestration and vascular injury induced by E. coli sepsis , 2005 .

[4]  Emilio Hirsch,et al.  Blockade of PI3Kγ suppresses joint inflammation and damage in mouse models of rheumatoid arthritis , 2005, Nature Medicine.

[5]  D. F. Barber,et al.  PI3Kγ inhibition blocks glomerulonephritis and extends lifespan in a mouse model of systemic lupus , 2005, Nature Medicine.

[6]  K. Okkenhaug,et al.  Sequential activation of class IB and class IA PI3K is important for the primed respiratory burst of human but not murine neutrophils. , 2005, Blood.

[7]  J. Penninger,et al.  The role of endothelial PI3Kgamma activity in neutrophil trafficking. , 2005, Blood.

[8]  Zhìhóng Hú,et al.  Activation of PI3-kinase/PKB contributes to delay in neutrophil apoptosis after thermal injury. , 2005, American journal of physiology. Cell physiology.

[9]  W. Chiou,et al.  C5a differentially stimulates the ERK1/2 and p38 MAPK phosphorylation through independent signaling pathways to induced chemotactic migration in RAW264.7 macrophages. , 2004, International immunopharmacology.

[10]  P. Ward,et al.  Regulatory Role of C5a on Macrophage Migration Inhibitory Factor Release from Neutrophils1 , 2004, The Journal of Immunology.

[11]  Ursula Bommhardt,et al.  Akt Decreases Lymphocyte Apoptosis and Improves Survival in Sepsis1 , 2004, The Journal of Immunology.

[12]  T. Graf,et al.  Mechanisms and implications of phosphoinositide 3-kinase delta in promoting neutrophil trafficking into inflamed tissue. , 2004, Blood.

[13]  J. V. Sarma,et al.  Regulatory role of C5a in LPS‐induced IL‐6 production by neutrophils during sepsis , 2004, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[14]  P. Ward The dark side of C5a in sepsis , 2004, Nature Reviews Immunology.

[15]  J. Kalbfleisch,et al.  Modulation of the Phosphoinositide 3-Kinase Pathway Alters Innate Resistance to Polymicrobial Sepsis 1 , 2004, The Journal of Immunology.

[16]  B. Jaber,et al.  C5a delays apoptosis of human neutrophils via an extracellular signal‐regulated kinase and Bad‐mediated signalling pathway , 2004, European journal of clinical investigation.

[17]  J. Paulauskis,et al.  Neutrophil C5a receptor and the outcome in a rat model of sepsis , 2003, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[18]  D. Staunton,et al.  Selective role of PI3Kδ in neutrophil inflammatory responses , 2003 .

[19]  P. Ward,et al.  Regulation by C5a of neutrophil activation during sepsis. , 2003, Immunity.

[20]  J. Klein,et al.  Akt Phosphorylates p47phox and Mediates Respiratory Burst Activity in Human Neutrophils1 , 2003, The Journal of Immunology.

[21]  Peter A. Ward,et al.  Novel strategies for the treatment of sepsis , 2003, Nature Medicine.

[22]  D. Staunton,et al.  Essential Role of Phosphoinositide 3-Kinase δ in Neutrophil Directional Movement , 2003, The Journal of Immunology.

[23]  John D Lambris,et al.  Protection of innate immunity by C5aR antagonist in septic mice , 2002, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[24]  J. V. Sarma,et al.  Complement-Induced Impairment of Innate Immunity During Sepsis1 , 2002, The Journal of Immunology.

[25]  John D Lambris,et al.  Essential role of the C5a receptor in E coli-induced oxidative burst and phagocytosis revealed by a novel lepirudin-based human whole blood model of inflammation. , 2002, Blood.

[26]  N. Mackman,et al.  The Phosphatidylinositol 3-Kinase-Akt Pathway Limits Lipopolysaccharide Activation of Signaling Pathways and Expression of Inflammatory Mediators in Human Monocytic Cells* , 2002, The Journal of Biological Chemistry.

[27]  John D Lambris,et al.  Increased C5a receptor expression in sepsis. , 2002, The Journal of clinical investigation.

[28]  Dianqing Wu,et al.  Neutrophils lacking phosphoinositide 3-kinase γ show loss of directionality during N-formyl-Met-Leu-Phe-induced chemotaxis , 2002, Proceedings of the National Academy of Sciences of the United States of America.

[29]  B. Jaber,et al.  C5a delays apoptosis of human neutrophils by a phosphatidylinositol 3-kinase-signaling pathway. , 2002, Kidney international.

[30]  J. Klein,et al.  Role of extracellular signal-regulated kinase and phosphatidylinositol-3 kinase in chemoattractant and LPS delay of constitutive neutrophil apoptosis. , 2001, Cellular signalling.

[31]  J. Klein,et al.  Granulocyte-Macrophage Colony-Stimulating Factor Delays Neutrophil Constitutive Apoptosis Through Phosphoinositide 3-Kinase and Extracellular Signal-Regulated Kinase Pathways1 , 2000, The Journal of Immunology.

[32]  Silvano Sozzani,et al.  Central role for G protein-coupled phosphoinositide 3-kinase γ in inflammation , 2000 .

[33]  G. Shankar,et al.  Bacterial lipopolysaccharide induced B cell activation is mediated via a phosphatidylinositol 3-kinase dependent signaling pathway. , 1999, Immunology letters.

[34]  P. Ward,et al.  Protective effects of C5a blockade in sepsis , 1999, Nature Medicine.

[35]  C. Tseng,et al.  A Requirement for Phosphatidylinositol 3-Kinase in Pseudopod Extension* , 1999, The Journal of Biological Chemistry.

[36]  J. Solomkin,et al.  Neutrophil dysfunction in sepsis. II. Evidence for the role of complement activation products in cellular deactivation. , 1981, Surgery.

[37]  P. Ward,et al.  Role of C5a in inflammatory responses. , 2005, Annual review of immunology.

[38]  M. Gadina,et al.  Kinase B / Akt Pathway and JNK Phosphatidylinositol 3-Kinase-Protein 3 Production Is Mediated by Activation of the-Protein-Dependent Inhibition of IL-12 iG , 2005 .