Crosstalk of signalling processes of innate immunity with Yersinia Yop effector functions

Immunobiology
Klaus RuckdeschelRudolf Haase

Abstract

The interaction of microbial pathogens with host cells critically determines the genesis of infectious diseases. Gram-negative, pathogenic bacteria from the genus Yersinia deliver a set of virulence proteins, the so-called Yersinia outer proteins (Yops), inside the eukaryotic cell where the Yops perturb key cellular functions of innate immunity. In our past work, we used Yersinia enterocolitica as a tool to explore the crosstalk between the bacterial pathogen and its host cell. Yersiniae counteract phagocytosis, suppress proinflammatory signalling and trigger apoptosis in macrophages. Macrophage cell death results from the deregulation of Toll-like receptors-dependent conserved signalling pathways by Yersinia infection. We summarize our current understanding about the signals and reactions elicited on both the bacterial and host cell sides that determine the fate of the infected cell along with the innate immune response.

References

Sep 18, 1997·Proceedings of the National Academy of Sciences of the United States of America·D M MonackS Falkow
Dec 8, 1998·The Journal of Experimental Medicine·D M MonackS Falkow
Jul 6, 2000·The EMBO Journal·A O AliprantisA Zychlinsky
Jan 5, 2002·The Journal of Biological Chemistry·Douglas D BannermanJohn M Harlan
Mar 5, 2002·Nature Immunology·Michael Karin, Anning Lin
Mar 23, 2002·Molecular and Cellular Biology·Kevin G LeongAly Karsan
Jun 27, 2002·Biochemical and Biophysical Research Communications·Douglas D BannermanJohn M Harlan
Oct 3, 2002·Nature Reviews. Molecular Cell Biology·Guy R Cornelis
Mar 26, 2003·Cell Death and Differentiation·H WajantP Scheurich
May 27, 2003·Nature Reviews. Immunology·Naohiro Inohara, Gabriel Nuñez
Jul 18, 2003·American Journal of Physiology. Cell Physiology·Mònica ComaladaAntonio Celada
Aug 6, 2003·Current Opinion in Immunology·Elizabeth Kopp, Ruslan Medzhitov
Sep 10, 2003·Journal of Leukocyte Biology·B BeutlerR J Ulevitch
Apr 6, 2004·Nature Immunology·Etienne MeylanJürg Tschopp
Jul 2, 2004·Nature Reviews. Immunology·Shizuo Akira, Kiyoshi Takeda
Apr 26, 2005·Annual Review of Microbiology·Gloria I Viboud, James B Bliska
Aug 2, 2005·Nature Cell Biology·Zhijian J Chen
Sep 24, 2005·The Journal of Biological Chemistry·Ying ZhangDaoguo Zhou
Nov 23, 2005·The Journal of Experimental Medicine·Honglin ZhouVishva M Dixit
Mar 7, 2006·PLoS Pathogens·Masmudur M Rahman, Grant McFadden
Nov 18, 2006·Nature Immunology·Jörg H FritzStephen E Girardin
Nov 23, 2006·Proceedings of the National Academy of Sciences of the United States of America·Rohit MittalHarvey T McMahon
Dec 23, 2006·Cell Death and Differentiation·J da Silva CorreiaR J Ulevitch

❮ Previous
Next ❯

Citations

Nov 20, 2013·Microbes and Infection·Mahesh Shanker Dhar, Jugsharan Singh Virdi
Aug 18, 2009·Cellular Microbiology·Anna FahlgrenMaria Fällman
Feb 26, 2011·Immunological Reviews·Annette PlüddemannSiamon Gordon
Nov 2, 2014·Cellular Microbiology·Peter M MerrittMelanie M Marketon
Jan 18, 2018·Letters in Applied Microbiology·S M HorneB M Prüβ
Jul 19, 2017·The Journal of Immunology : Official Journal of the American Association of Immunologists·Roberto C DavicinoGabriel A Rabinovich
Mar 6, 2018·BMC Genomics·Olga L VoroninaAlexandr L Gintsburg
Oct 9, 2009·The Journal of Immunology : Official Journal of the American Association of Immunologists·Anne DeuretzbacherKlaus Ruckdeschel

❮ Previous
Next ❯

Related Concepts

Related Feeds

ApoE, Lipids & Cholesterol

Serum cholesterol, triglycerides, apolipoprotein B (APOB)-containing lipoproteins (very low-density lipoprotein (VLDL), immediate-density lipoprotein (IDL), and low-density lipoprotein (LDL), lipoprotein A (LPA)) and the total cholesterol/high-density lipoprotein (HDL) cholesterol ratio are all connected in diseases. Here is the latest research.

Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis