Crosstalk of signalling processes of innate immunity with Yersinia Yop effector functions.
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Crosstalk of signalling processes of innate immunity with Yersinia Yop effector functions. / Ruckdeschel, Klaus; Deuretzbacher, Anne; Haase, Rudolf.
in: IMMUNOBIOLOGY, Jahrgang 213, Nr. 3-4, 3-4, 2008, S. 261-269.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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TY - JOUR
T1 - Crosstalk of signalling processes of innate immunity with Yersinia Yop effector functions.
AU - Ruckdeschel, Klaus
AU - Deuretzbacher, Anne
AU - Haase, Rudolf
PY - 2008
Y1 - 2008
N2 - 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.
AB - 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.
M3 - SCORING: Zeitschriftenaufsatz
VL - 213
SP - 261
EP - 269
JO - IMMUNOBIOLOGY
JF - IMMUNOBIOLOGY
SN - 0171-2985
IS - 3-4
M1 - 3-4
ER -
