Effector functions of pathogenic Yersinia species

被引：27

作者：

Aepfelbacher, Martin ^{[1
]}

Trasak, Claudia ^{[1
]}

Ruckdeschel, Klaus ^{[1
]}

机构：

[1] Univ Klinikum Eppendorf, Diagnost Zentrum, Inst Med Mikrobiol Virol & Hyg, D-20246 Hamburg, Germany

来源：

THROMBOSIS AND HAEMOSTASIS | 2007年 / 98卷 / 03期

关键词：

Yersinia; Yops; Rho; GTPases; signalling; anti-inflammation; apoptosis;

D O I：

10.1160/TH07-03-0173

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Pathogenic species of the genus Yersinia suppress and reorient the immune system to infect lymphatic tissues, inner organs and at times also the vasculature. For this purpose yersiniae employ a type III secretion system to translocate effector proteins (Yersinia outer proteins; Yops) into immune cells. Yops often exert unique biochemical activities for modulating the activity of Rho GTP-binding proteins, focal adhesion proteins, inflammatory pathways and cell survival/apoptosis. In this review we will put emphasis on the biochemistry, cell- and infection biology of Yersinia effector Yops.

引用

收藏

页码：521 / 529

页数：9

相关论文

共 105 条

[71] Yersinia virulence depends on mimicry of host Rho-family nucleotide dissociation inhibitors [J].

Prehna, Gerd ;

Ivanov, Maya I. ;

Bliska, James B. ;

Stebbins, C. Erec .

CELL, 2006, 126 (05) :869-880

[72] YERSINIA-PESTIS YOPM - THROMBIN BINDING AND OVEREXPRESSION [J].

REISNER, BS ;

STRALEY, SC .

INFECTION AND IMMUNITY, 1992, 60 (12) :5242-5252

[73] The weak interaction of LcrV and TLR2 does not contribute to the virulence of Yersinia pestis [J].

Reithmeier-Rost, Dagmar ;

Hill, Jim ;

Elvin, Stephen J. ;

Williamson, Diane ;

Dittmann, Svea ;

Schmid, Annika ;

Wilharm, Gottfried ;

Sing, Andreas .

MICROBES AND INFECTION, 2007, 9 (08) :997-1002

[74] INHIBITION OF PHAGOCYTOSIS IN YERSINIA-PSEUDOTUBERCULOSIS - A VIRULENCE PLASMID-ENCODED ABILITY INVOLVING THE YOP2B PROTEIN [J].

ROSQVIST, R ;

BOLIN, I ;

WOLFWATZ, H .

INFECTION AND IMMUNITY, 1988, 56 (08) :2139-2143

[75] Differential contribution of Yersinia enterocolitica virulence factors to evasion of microbicidal action of neutrophils [J].

Ruckdeschel, K ;

Roggenkamp, A ;

Schubert, S ;

Heesemann, J .

INFECTION AND IMMUNITY, 1996, 64 (03) :724-733

[76]

Ruckdeschel K, 2002, ARCH IMMUNOL THER EX, V50, P131

[77] Signaling of apoptosis through TLRs critically involves toll/IL-1 receptor domain-containing adapter inducing IFN-β, but not MyD88, in bacteria-infected murine macrophages [J].

Ruckdeschel, K ;

Pfaffinger, G ;

Haase, R ;

Sing, A ;

Weighardt, H ;

Häcker, G ;

Holzmann, B ;

Heesemann, J .

JOURNAL OF IMMUNOLOGY, 2004, 173 (05) :3320-3328

[78] Yersinia outer protein P of Yersinia enterocolitica simultaneously blocks the nuclear factor-κB pathway and exploits lipopolysaccharide signaling to trigger apoptosis in macrophages [J].

Ruckdeschel, K ;

Mannel, O ;

Richter, K ;

Jacobi, CA ;

Trülzsch, K ;

Rouot, B ;

Heesemann, J .

JOURNAL OF IMMUNOLOGY, 2001, 166 (03) :1823-1831

[79] The proteasome pathway destabilizes Yersinia outer protein E and represses its antihost cell activities [J].

Ruckdeschel, Klaus ;

Pfaffinger, Gudrun ;

Truelzsch, Konrad ;

Zenner, Gerhardt ;

Richter, Kathleen ;

Heesemann, Juergen ;

Aepfelbacher, Martin .

JOURNAL OF IMMUNOLOGY, 2006, 176 (10) :6093-6102

[80] Regulation of mRNA expression in macrophages after Yersinia enterocolitica infection -: Role of different Yop effectors [J].

Sauvonnet, N ;

Pradet-Balade, B ;

Garcia-Sanz, JA ;

Cornelis, GR .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2002, 277 (28) :25133-25142

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