Signaling by Myeloid C-Type Lectin Receptors in Immunity and Homeostasis

Author:

Sancho David1,Reis e Sousa Caetano2

Affiliation:

1. Department of Vascular Biology and Inflammation, CNIC, Centro Nacional de Investigaciones Cardiovasculares, E-28029, Madrid, Spain;

2. Immunobiology Laboratory, Cancer Research UK, London Research Institute, Lincoln's Inn Fields Laboratories, London WC2A 3LY, United Kingdom;

Abstract

Myeloid cells are key drivers of physiological responses to pathogen invasion or tissue damage. Members of the C-type lectin receptor (CLR) family stand out among the specialized receptors utilized by myeloid cells to orchestrate these responses. CLR ligands include carbohydrate, protein, and lipid components of both pathogens and self, which variably trigger endocytic, phagocytic, proinflammatory, or anti-inflammatory reactions. These varied outcomes rely on a versatile system for CLR signaling that includes tyrosine-based motifs that recruit kinases, phosphatases, or endocytic adaptors as well as nontyrosine-based signals that modulate the activation of other pathways or couple to the uptake machinery. Here, we review the signaling properties of myeloid CLRs and how they impact the role of myeloid cells in innate and adaptive immunity.

Publisher

Annual Reviews

Subject

Immunology,Immunology and Allergy

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