Effector-Triggered Immunity

Author:

Remick Brenna C.1,Gaidt Moritz M.2,Vance Russell E.13

Affiliation:

1. Division of Immunology and Molecular Medicine, Department of Molecular and Cell Biology, University of California, Berkeley, California, USA

2. Research Institute of Molecular Pathology, Vienna BioCenter, Vienna, Austria

3. Howard Hughes Medical Institute, University of California, Berkeley, California, USA;

Abstract

The innate immune system detects pathogens via germline-encoded receptors that bind to conserved pathogen ligands called pathogen-associated molecular patterns (PAMPs). Here we consider an additional strategy of pathogen sensing called effector-triggered immunity (ETI). ETI involves detection of pathogen-encoded virulence factors, also called effectors. Pathogens produce effectors to manipulate hosts to create a replicative niche and/or block host immunity. Unlike PAMPs, effectors are often diverse and rapidly evolving and can thus be unsuitable targets for direct detection by germline-encoded receptors. Effectors are instead often sensed indirectly via detection of their virulence activities. ETI is a viable strategy for pathogen sensing and is used across diverse phyla, including plants, but the molecular mechanisms of ETI are complex compared to simple receptor/ligand-based PAMP detection. Here we survey the mechanisms and functions of ETI, with a particular focus on emerging insights from animal studies. We suggest that many examples of ETI may remain to be discovered, hiding in plain sight throughout immunology.

Publisher

Annual Reviews

Subject

Immunology,Immunology and Allergy

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