[1] SINGER M, DEUTSCHMAN C S, SEYMOUR C W, et al.The third international consensus definitions for sepsis and septic shock(Sepsis-3)[J].JAMA, 2016, 315(8):801-810.
[2] FLEISCHMANN C, SCHERAG A, ADHIARI N K, et al.Assessment of global incidence and mortality of hospital-treated sepsis.Current estimates and limitations[J].Am J Respir Crit Care Med, 2016, 193(3):259-272.
[3] JACOBS L, BERRENS Z, STENSON E K, et al.Interleukin-27 as a candidate diagnostic biomarker for bacterial infection in immunocompromised pediatric patients[J].PLoS One, 2018, 13(11):e0207620.
[4] YOSHIDA H, HUNTER C A.The immunobiology of interleukin-27[J].Annu Rev Immunol, 2015, 33:417-443.
[5] LIU J, GUAN X, MA X.Regulation of IL-27 p28 gene expression in macrophages through MyD88-and interferon-gamma-mediated pathways[J].J Exp Med, 2007, 204(1):141-152.
[6] VIGNALI D A, KUCHROO V K.IL-12 family cytokines:immunological playmakers[J].Nat Immunol, 2012, 13(8):722-728.
[7] POVROZNIK J M, ROBINSON C M.IL-27 regulation of innate immunity and control of microbial growth[J].Future Sci OA, 2020, 6(7):Fso588.
[8] KALLIOLIAS G D, GORDON R A, IVASHKIV L B.Suppression of TNF-α and IL-1 signaling identifies a mechanism of homeostatic regulation of macrophages by IL-27[J].J Immunol, 2010, 185(11):7047-7056.
[9] COX J H, KLJAVIN N M, RAMAMOORTHI N, et al.IL-27 promotes T cell-dependent colitis through multiple mechanisms[J].J Exp Med, 2011, 208(1):115-123.
[10] BATTEN M, LI J, YI S, et al.Interleukin 27 limits autoimmune encephalomyelitis by suppressing the development of interleukin 17-producing T cells[J].Nat Immunol, 2006, 7(9):929-936.
[11] PETES C, MINTSOPOULOS V, FINNEN R L, et al.The effects of CD14 and IL-27 on induction of endotoxin tolerance in human monocytes and macrophages[J].J Biol Chem, 2018, 293(45):17631-17645.
[12] GUZZO C, AYER A, BASTA S, et al.IL-27 enhances LPS-induced proinflammatory cytokine production via upregulation of TLR4 expression and signaling in human monocytes[J].J Immunol, 2012, 188(2):864-873.
[13] YOSHIDA H, HAMANO S, SENALDI G, et al.WSX-1 is required for the initiation of Th1 responses and resistance to L.major infection[J].Immunity, 2001, 15(4):569-578.
[14] VAN A H, COENYE T.The Role of reactive oxygen species in antibiotic-mediated killing of bacteria[J].Trends Microbiol, 2017, 25(6):456-466.
[15] SHESHACHALAM A, SRIVASTAVA N, MITCHELL T, et al.Granule protein processing and regulated secretion in neutrophils[J].Front Immunol, 2014, 5:448.
[16] NGUYEN G T, GREEN E R, MECSAS J.Neutrophils to the ROScue:mechanisms of NADPH oxidase activation and bacterial resistance[J].Front Cell Infect Microbiol, 2017, 7:373.
[17] SANTOS S S, BRUNIALTI M K, RIGATO O, et al.Generation of nitric oxide and reactive oxygen species by neutrophils and monocytes from septic patients and association with outcomes[J].Shock, 2012, 38(1):18-23.
[18] WANG H, SUN X, LU Q, et al.The mitochondrial redistribution of eNOS is involved in lipopolysaccharide induced inflammasome activation during acute lung injury[J].Redox Biol, 2021, 41:101878.
[19] YANG H, ZHANG Z.Sepsis-induced myocardial dysfunction:the role of mitochondrial dysfunction[J].Inflamm Res, 2021, 70(4):379-387.
[20] JENSEN I J, MCGONAGILL P W, BERTON R R, et al.Prolonged reactive oxygen species production following septic insult[J].Immunohorizons, 2021, 5(6):477-488.
[21] LI J P, WU H, XING W, et al.Interleukin-27 as a negative regulator of human neutrophil function[J].Scand J Immunol, 2010, 72(4):284-292.
[22] WIRTZ S, BECKER C, FANTINI M C, et al.EBV-induced gene 3 transcription is induced by TLR signaling in primary dendritic cells via NF-kappa B activation[J].J Immunol, 2005, 174(5):2814-2824.
[23] WIRTZ S, TUBBE I, GALLE P R, et al.Protection from lethal septic peritonitis by neutralizing the biological function of interleukin 27[J].J Exp Med, 2006, 203(8):1875-1881.
[24] RINCHAI D, KHAENAM P, KEWCHAROENWONG C, et al.Production of interleukin-27 by human neutrophils regulates their function during bacterial infection[J].Eur J Immunol, 2012, 42(12):3280-3290.
[25] STROBE B, STOIBER D, SEXL V, et al.Tyrosine kinase 2(TYK2) in cytokine signalling and host immunity[J].Front Biosci(Landmark Ed), 2011, 16(9):3214-3232.
[26] FUCHS S, KAISER L P, BANK J, et al.Tyrosine kinase 2 is not limiting human antiviral type III interferon responses[J].Eur J Immunol, 2016, 46(11):2639-2649.
[27] POELZL A, LASSNIG C, TANGERMANN S, et al.TYK2 licenses non-canonical inflammasome activation during endotoxemia[J].Cell Death Differ, 2021, 28(2):748-763.
[28] VOGL C, FLATT T, FUHRMANN B, et al.Transcriptome analysis reveals a major impact of JAK protein tyrosine kinase 2(Tyk2) on the expression of interferon-responsive and metabolic genes[J].BMC Genomics, 2010, 11:199.
[29] BOSMANN M, STROBE B, KICHLER N, et al.Tyrosine kinase 2 promotes sepsis-associated lethality by facilitating production of interleukin-27[J].J Leukoc Biol, 2014, 96(1):123-131.
[30] BOSMANN M, HAGGADONE M D, HEMMILA M R, et al.Complement activation product C5a is a selective suppressor of TLR4-induced, but not TLR3-induced, production of IL-27(p28) from macrophages[J].J Immunol, 2012, 188(10):5086-5093.
[31] CABRERA E, HERNANDEZ P S, KOUNDRIOUKOFF S, et al.PERK inhibits DNA replication during the Unfolded Protein Response via Claspin and Chk1[J].Oncogene, 2017, 36(5):678-686.
[32] LI S T, DAI Q, ZHANG S X, et al.Ulinastatin attenuates LPS-induced inflammation in mouse macrophage RAW264.7 cells by inhibiting the JNK/NF-κB signaling pathway and activating the PI3K/Akt/Nrf2 pathway[J].Acta Pharmacol Sin, 2018, 39(8):1294-1304.
[33] SABAPATHY K.Role of the JNK pathway in human diseases[J].Prog Mol Biol Transl Sci, 2012, 106:145-169.
[34] 李青青, 陆刚, 丁怿虹, 等.脓毒症诱导小鼠淋巴器官JNK和CHOP凋亡途径及刺激炎性细胞因子的变化[J].中华危重病急救医学, 2020, 32(10):1194-1198.
[35] NIE Z, XIA X, ZHAO Y, et al.JNK selective inhibitor, IQ-1S, protects the mice against lipopolysaccharides-induced sepsis[J].Bioorg Med Chem, 2021, 30:115945.
[36] LOU L, HU D, CHEN S, et al.Protective role of JNK inhibitor SP600125 in sepsis-induced acute lung injury[J].Int J Clin Exp Pathol, 2019, 12(2):528-538.
[37] BAUER M, PRESS A T, TRAUNER M.The liver in sepsis:patterns of response and injury[J].Curr Opin Crit Care, 2013, 19(2):123-127.
[38] FAN J, ZHANG Y C, ZHENG D F, et al.IL-27 is elevated in sepsis with acute hepatic injury and promotes hepatic damage and inflammation in the CLP model[J].Cytokine, 2020, 127:154936.
[39] CHANG X, HU L F, MA X J, et al.Influence of roflumilast on sepsis mice through the JAK/STAT signaling pathway[J].Eur Rev Med Pharmacol Sci, 2019, 23(3):1335-1341.
[40] HILLMER E J, ZHANG H, LI H S, et al.STAT3 signaling in immunity[J].Cytokine Growth Factor Rev, 2016, 31:1-15.
[41] FABBI M, CARBOTTI G, FERRINI S.Dual roles of IL-27 in cancer biology and immunotherapy[J].Mediators Inflamm, 2017, 2017:3958069.
[42] ZHOU P, DENG B, WU M, et al.Interleukin-27 Ameliorates renal ischemia-reperfusion injury through signal transducers and activators of transcription 3 signaling pathway[J].Kidney Blood Press Res, 2019, 44(6):1453-1464.
[43] 巫霞, 任妍, 巫慧敏.IL-27通过STAT3信号通路改善脂多糖诱导的小鼠急性肺炎[J].温州医科大学学报, 2020, 50(4):317-322, 327.
[44] BOSMANN M, RUSSKAMP N F, STROBL B, et al.Interruption of macrophage-derived IL-27(p28) production by IL-10 during sepsis requires STAT3 but not SOCS3[J].J Immunol, 2014, 193(11):5668-5677.
[45] MONNEY L, SABOTOS C A, GAGLIA J L, et al.Th1-specific cell surface protein Tim-3 regulates macrophage activation and severity of an autoimmune disease[J].Nature, 2002, 415(6871):536-541.
[46] XIA Q, WEI L, ZHANG Y, et al.Immune checkpoint receptors Tim-3 and PD-1 regulate monocyte and T lymphocyte function in septic patients[J].Mediators Inflamm, 2018, 2018:1632902.
[47] KADOWAKI T, MORISHITA A, NIKI T, et al.Galectin-9 prolongs the survival of septic mice by expanding Tim-3-expressing natural killer T cells and PDCA-1+ CD11c+ macrophages[J].Crit Care, 2013, 17(6):R284.
[48] YAO Y, DENG H, LI P, et al.α-Lactose improves the survival of septic mice by blockade of TIM-3 signaling to prevent NKT cell apoptosis and attenuate cytokine storm[J].Shock, 2017, 47(3):337-345.
[49] ZHU C, SAKUISHI K, XIAO S, et al.An IL-27/NFIL3 signalling axis drives Tim-3 and IL-10 expression and T-cell dysfunction[J].Nat Commun, 2015, 6:6072. |
