[1]Benedyk M, Mydel PM, Delaleu N, et al.Gingipains: Critical Factors in the Development of Aspiration Pneumonia Caused by Porphyromonas gingivalis[J].J Innate Immun, 2016, 8(2):185-98[2] Pockpa ZA, Struillou X, Coulibaly NT, et al.Potential relationship between periodontal diseases and eye diseases [J]. Med Hypotheses, 2017, 99: 63-66.[3]Perrotta M, Lembo G, Carnevale D.The Multifaceted Roles of PI3Kγ in Hypertension,Vascular Biology,and Inflammation[J].Int J Mol Sci, 2016, 17(11):1858-[4] Okkenhaug K.Signalling by the phosphoinositide 3-kinase family in immune cells [J]. AAnnu Rev Immunol, 2013, 31:675-704.[5]Vanhaesebroeck B, Guillermet-Guibert J, Graupera M, et al.The emerging mechanisms of isoform-specific PI3K signalling[J].Nat Rev Mol Cell Biol, 2010, 11(5):329-41[6]Juss JK, Hayhoe RP, Owen CE, et al.Functional redundancy of class I phosphoinositide 3-kinase (PI3K) isoforms in signaling growth factor-mediated human neutrophil survival[J].PLoS One, 2012, 7(9):e45933-[7]Vanhaesebroeck B, Stephens L, Hawkins P.PI3K signalling: the path to discovery and understanding[J].Nat Rev Mol Cell Biol, 2012, 13(3):195-203[8]Martini M, De Santis MC, Braccini L, et al.PI3KAKT signaling pathway and cancer: an updated review[J].Ann Med, 2014, 46(6):372-83[9]Katholnig K, Linke M, Pham H, et al.Immune responses of macrophages and dendritic cells regulated by mTOR signalling[J].Biochem Soc Trans, 2013, 41(4):927-33[10]Lawrence T, Natoli G.Transcriptional regulation of macrophage polarization: enabling diversity with identity[J].Nat Rev Immunol, 2011, 11(11):750-61[11]Liu Y, Zhu H, Su Z, et al.IL-17 contributes to cardiac fibrosis following experimental autoimmune myocarditis by a PKCβErk12NF-κB-dependent signaling pathway[J].Int Immunol, 2012, 4(10):605-12[12]Su Z, Sun C, Zhou C, et al.HMGB1 blockade attenuates experimental autoimmune myocarditis and suppresses Th17‐cell expansion[J].Eur J Immunol, 2011, 41(12):3586-95[13]Su Z, Yin J, Wang T, et al.Up‐regulated HMGB1 in EAM directly led to collagen deposition by a PKCβErk12‐dependent pathway: cardiac fibroblastmyofibroblast might be another source of HMGB1[J].J Cell Mol Med, 2014, 18(9):1740-51[14] Su Z, Zhang P, Yu Y, et al.HMGB1 Facilitated Macrophage Reprogramming towards a Proinflammatory M1-like Phenotype in Experimental Autoimmune Myocarditis Development [J]. Sci Rep, 2016, 6:21884.[15]Kaneda MM, Messer KS, Ralainirina N, et al.PI3Kγ is a molecular switch that controls immune suppression[J].Nature, 2016, 539(7629):437-442[16]Ben-Neriah Y, Karin M.Inflammation meets cancer,with NF-[kappa] B as the matchmaker[J].Nat Immunol, 2011, 12(8):715-23[17]Poli V.The role of CEBP isoforms in the control of inflammatory and native immunity functions[J].J Biol Chem, 1998, 273(45):29279-82[18]Gray M J, Poljakovic M, Kepka-Lenhart D, et al.Induction of arginase I transcription by IL-4 requires a composite DNA response element for STAT6 and CEBPβ[J].Gene, 2005, 353(1):98-106[19]Ashigaki N, Suzuki J, Ogawa M, et al.Periodontal bacteria aggravate experimental autoimmune myocarditis in mice[J].Am J Physiol Heart Circ Physiol, 2013, 304(5):H740-8[20]Lam RS, O' Brien-Simpson NM, Lenzo JC, et al.Macrophage depletion abates Porphyromonas gingivalis-induced alveolar bone resorption in mice[J].J Immunol, 2014, 193(5):2349-62[21]Tipton DA, Cho S, Zacharia N, et al.Inhibition of interleukin-17-stimulated interleukin-6 and -8 production by cranberry components in human gingival fibroblasts and epithelial cells[J].J Periodontal Res, 2013, 48(5):638-46[22]Yu T, Zhao L, Huang X, et al.Enhanced Activity of the Macrophage M1M2 Phenotypes and Phenotypic Switch to M1 in Periodontal Infection[J].J Periodontol, 2016, 87(9):1092-102[23] Luo L, Wall AA, Yeo J C, et al.Rab8a interacts directly with PI3Kγ to modulate TLR4-driven PI3K and mTOR signalling [J]. Nat Commun, 2014, 5:4407.[24]Hattula K, Furuhjelm J, Tikkanen J, et al.Characterization of the Rab8-specific membrane traffic route linked to protrusion formation[J].J Cell Sci, 2006, 119(Pt 23):4866-77[25]Weichhart T, S?emann MD.The multiple facets of mTOR in immunity[J].Trends Immunol, 2009, 30(5):218-26[26]Holden JA, Attard TJ, Laughton KM et al.Porphyromonas gingivalis lipopolysaccharide weakly activates M1 and M2 polarized mouse macrophages but induces inflammatory cytokines[J].Infect Immun, 2014, 82(10):4190-203 |