[1] ATLURI V L,XAVIER M N,DE JONG M F,et al.Interactions of the human pathogenic Brucella species with their hosts[J].Annual Review of Microbiology,2011,65(1):523-541.
[2] 易德武,张俊波,王远志,等.羊种布鲁氏菌新疆流行株015株sodc基因缺失株的构建与初步评价[J].石河子大学学报(自然科学版),2016,34(1):24-29. YI D W,ZHANG J B,WANG Z Y,et al.Construction and identification o Brucella melitensis in Xinjiang epidemic strain 015sodc gene dele tion strains[J].Journal of Shihezi University (Natural Science),2016,34(1):24-29.(in Chinese)
[3] 董炳梅,王金良,唐娜,等.布鲁氏菌的致病机制与细胞免疫机制研究进展[J].中国人兽共患病学报,2012,28(6):635-639. DONG B M,WANG J L,TANG N,et al.Progress in pathogenesis and cellular immune mechanism of Brucella[J].Chinese Journal of Zoonoses,2012,28(6):635-639.(in Chinese)
[4] 宛硕,黄艳,陈庭金,等.巨噬细胞极化的研究进展[J].中国病原生物学杂志,2015,11:1051-1054. WAN S,HUANG Y,CHEN T J,et al.Progress in research of macrophage polarization[J].Journal of Pathogen Biology,2015,11:1051-1054.(in Chinese)
[5] CHEN Q,LAI S,YIN W,et al.Epidemic characteristics,high-risk townships and spacetime clusters of human brucellosis in Shanxi province of China[J].BMC Infectious Diseases,2016,16(1):760.
[6] GLASS C K,NATOLI G.Molecular control of activation and priming in macrophages[J].Nature Immunology,2016,17(1):26-33.
[7] HOEBE K,JANSSEN E,BEUTLER B.The interface between innate and adaptive immunity[J].Nature Immunology,2004,5(10):971-974.
[8] 王乐怡,吴欣怡.Toll样受体与NOD样受体在炎症中作用的研究进展[J].现代免疫学,2010,30(5):436-439. WANG L Y,WU X Y.Progress in the role of Toll like receptors and NOD like receptors in inflamma-tion[J].Current Immunology,2010,30(5):436-439.(in Chinese)
[9] MARTIROSYAN A,MORENO E,GORVEL J P.An evolutionary strategy for a stealthy intracellular Brucella pathogen[J].Immunological Reviews,2011,240(1):211-234.
[10] LAPAQUE N,TAKEUCHI O,CORRALES F,et al.Differential inductions of TNF-alpha and IGTP,ⅡGP by structurally diverse classic and non-classic lipopolysaccharides[J].Cellular Microbiology,2006,8(3):401-413.
[11] RAQUEL C Á,VILMA A G,MAITE I,et al.The lipopolysaccharide core of Brucella abortus acts as a shield against innate immunity recognition[J].PLoS Pathogens,2012,8(5):e1002675.
[12] BARQUERO-CALVO E,CHAVES-OLARTE E,WEISS D S,et al.Brucella abortus uses a stealthy strategy to avoid activation of the innate immune system during the onset of infection[J].PLoS One,2007,2(7):e631.
[13] WILSON R P,WINTER S E,SPEES A M,et al.The Vi capsular polysaccharide prevents complement receptor 3-mediated clearance of Salmonella enterica serotype Typhi[J].Infection & Immunity,2011,79(2):830-837.
[14] BARQUERO-CALVO E,MORA-CARTIN R,ARCE-GORVEL V,et al.Brucella abortus induces the premature death of human neutrophils through the action of its lipopolysaccharide[J].PLoS Pathogens,2015,11(5):e1004853.
[15] ROLAN H G,TSOLIS R M.Inactivation of the type Ⅳ secretion system reduces the Th1 polarization of the immune response to Brucella abortus infection[J].Infection & Immunity,2008,76(7):3207-3213.
[16] GOMES M T,CAMOS P C,OlIVEIRA F S,et al.Critical role of ASC inflammasomes and bacterial typeⅣsecretion system in caspase-1 activation and host innate resistance to Brucella abortus infection[J].Journal of Immunology,2013,190(7):3629-3638.
[17] 权伍荣,杨咏洁.布鲁氏菌逃逸宿主的抗感染免疫机制[J].微生物学报,2016,56(5):747-752. QUAN W R,YANG Y J.The anti-infection immunity mechanism of Brucella escape host[J] Acta Microbiologica Sinica,2016,56(5):747-752.(in Chinese)
[18] CLOECKAERT A,VIZCAINO N,PAQUET J Y,et al.Major outer membrane protein of Brucella spp.:Past,preseng,and future[J].Veterinary Microbiology,2002,90(1-4):229-247.
[19] PASQUEVICH K A,ESTEIN S M,GARCÍA SAMARTINO C,et al.Immunization with recombinant Brucella species outer membrane protein OMP16 or OMP19 in adjuvant induces specific CD4+ and CD8+ T cell as well as systemic and oral protection against Brucella abortus infection[J].Infection and Immunity,2009,77(1):436-445.
[20] SARAIVA M,O'GARRA A.The regulation of IL-10 production by immune cells[J].Nature Reviews Immunology,2010,10(3):170-181.
[21] XAVIER M N,WINTER M G,SPEES A M,et al.CD4+ T cell-derived IL-10 promotes Brucella abortus persistence via modulation of macrophage function[J].PLoS Pathogens,2013,9(6):e1003454.
[22] XAVIER M,WINTER M,SPEES A,et al.PPARγ-mediated increase in glucose availability sustains chronic Brucella abortus infection in alternatively activated macrophages[J].Cell Host & Microbe,2013,14(2):159-170.
[23] ZHOU L,CAO X,FANG J,et al.Macrophages polarization is mediated by the combination of PRR ligands and distinct inflammatory cytokines[J].International Journal of Clinical and Experimental Pathology,2015,8(9):10964-10974.
[24] EI KASMI K C,STENMARK K R.Contribution of metabolic reprogramming to macrophage plasticity and function[J].Seminars in Immunology,2015,27(4):267-275.
[25] NOVOSELOV V V,SAZONOVA M A,IVANOVA E A,et al.Study of the activated macrophage transcriptome[J].Experimental and Molecular Pathology,2015,99(3):575-580.
[26] FU C,JIANG L,XU X,et al.STAT4 knockout protects LPS-induced lung injury by increasing of MDSC and promoting of macrophage differentiation[J].Respiratory Physiology & Neurobiology,2015,223:16-22.
[27] STAITIEH B S,EGEA E E,FAN X,et al.Activation of alveolar macrophages with interferon-γ promotes antioxidant defenses via the Nrf2-ARE pathway[J].Journal of Clinical and Cellular Immunology,2015,6(5):365.
[28] YING W,TSENG A,CHANG C A,et al.microRNA-223 is a crucial mediator of PPARγ-regulated alternative macrophage activation[J].Journal of Clinical Investigation,2015,125(11):4149-4159.
[29] VERRECK F A,DE BOER T,LANGENBERG D M,et al.Human IL-23-producing type 1 macrophages promote but IL-10-producing type 2 macrophages subvert immunity to (myco) bacteria[J].Proceedings of the National Academy of Sciences of the United States of America,2004,101(13):4560-4565.
[30] LAWRENCE T,NATOLI G.Transcriptional regulation of macrophage polarization:Enabling diversity with identity[J].Nature Reviews Immunology, 2011,11(11):750-761.
[31] WU X,YANG Y,LI W,et al.Telomerase reverse transcriptase acts in a feedback loop with NF-κB pathway to regulate macrophage polarization in alcoholic liver disease[J].Scientific Reports,2016,6:18685.
[32] SU H,KONG C,ZHU L,et al.PPE26 induces TLR2-dependent activation of macrophages and drives Th1-type T-cell immunity by triggering the cross-talk of multiple pathways involved in the host respons[J].Oncotarget,2015,6(36):38517-38537.
[33] YANG C,ZHANG D M,SONG Z B,et al.Protumoral TSP 50 regulates macrophage activities and polarization via production of TNF-α and IL-1β,and activation of the NF-κB signaling pathway[J].PLoS One,2015,10(12):e0145095.
[34] 熊思东.疾病发病中的巨噬细胞极化:机制与作用[J].现代免疫学,2010,30(5):353-360. XIONG S D.Macrophage polarization in the pathogenesis of disease:Mechanism and function[J].Current Immunology,2010,30(5):353-360.(in Chinese)
[35] TIMMER A M,NIZET V.IKKβ/NF-κB and the miscreant macrophage[J].The Journal of Experimental Medicine,2008,205(6):1255-1259.
[36] GORDON S,MARTINEZ F O.Alternative activation of macrophages:Mechanism and functions[J].Immunity,2010,32(5):593-604.
[37] EVERTS B,AMIEL E,VAN DER WINDT G J,et al.Commitment to glycolysis sustains survival of NO-producing inflammatory dendritic cells[J].Blood,2012,120(7):1422.
[38] O'NEILL L A,HARDIE D G.Metabolism of inflammation limited by AMPK and pseudo-starvation[J].Nature,2013,493(7432):346-355.
[39] RODRIGUEZ-PRADOS J C,TRAVES P G,CUENCA J,et al.Substrate fate in activated macrophages:A comparison between innate,classic,and alternative activation[J].Journal of Immunology,2010,185(1):605-614.
[40] BENSINGERE S J,TONTONOZ P.Integration of metabolism and inflammation by lipid-activated nuclear receptors[J].Nature, 2008,454(7203):470-477.
[41] HONG P C,TSOLIS R M,FICHT T A.Identification of genes required for chronic persistence of Brucella abortus in mice[J].Infection & Immunity,2000,68(7):4102-4107.
[42] ROOP R M 2ND,CASWELL C C.Bacterial persistence:Finding the "sweet spot"[J].Cell Host & Microbe,2013,14(2):119-120.
[43] EISELE N A,RUBY T,JACOBSON A,et al.Salmonella require the fatty acid regulator PPARδ for the establishment of a metabolic environment essential for long term persistence[J].Cell Host & Microbe,2013,14(2):171-182.
[44] BARBIER T,NICOLAS C,LETESSON J J.Brucella adaptation and survival at the crossroad of metabolism and virulence[J].Febs Letters, 2011,585(19):2929-2934.
[45] FADOK V,BRATTON D,KONOWALL A,et al.Macrophages that have ingested apoptotic cells in vitro inhibit proinflammatory cytokine production through autocrine/paracrine mechanisms involving TGF-β,PGE2,and PAF[J].Journal of Clinical Investigation,1998,101(4):890-898. |