Pathogen-derived effectors trigger protective immunity via activation of the Rac2 enzyme and the IMD or Rip kinase signaling pathway.

Abstract:

:Although infections with virulent pathogens often induce a strong inflammatory reaction, what drives the increased immune response to pathogens compared to nonpathogenic microbes is poorly understood. One possibility is that the immune system senses the level of threat from a microorganism and augments the response accordingly. Here, focusing on cytotoxic necrotizing factor 1 (CNF1), an Escherichia coli-derived effector molecule, we showed the host indirectly sensed the pathogen by monitoring for the effector that modified RhoGTPases. CNF1 modified Rac2, which then interacted with the innate immune adaptors IMD and Rip1-Rip2 in flies and mammalian cells, respectively, to drive an immune response. This response was protective and increased the ability of the host to restrict pathogen growth, thus defining a mechanism of effector-triggered immunity that contributes to how metazoans defend against microbes with pathogenic potential.

journal_name

Immunity

journal_title

Immunity

authors

Boyer L,Magoc L,Dejardin S,Cappillino M,Paquette N,Hinault C,Charriere GM,Ip WK,Fracchia S,Hennessy E,Erturk-Hasdemir D,Reichhart JM,Silverman N,Lacy-Hulbert A,Stuart LM

doi

10.1016/j.immuni.2011.08.015

subject

Has Abstract

pub_date

2011-10-28 00:00:00

pages

536-49

issue

4

eissn

1074-7613

issn

1097-4180

pii

S1074-7613(11)00405-5

journal_volume

35

pub_type

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