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© Research
Publication : Frontiers in immunology

CR3 Engaged by PGL-I Triggers Syk-Calcineurin-NFATc to Rewire the Innate Immune Response in Leprosy

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in Frontiers in immunology - 17 Dec 2019

Doz-Deblauwe É, Carreras F, Arbues A, Remot A, Epardaud M, Malaga W, Mayau V, Prandi J, Astarie-Dequeker C, Guilhot C, Demangel C, Winter N

Link to Pubmed [PMID] – 31921172

Front Immunol 2019;10:2913

, the causative agent of leprosy, is unique amongst human pathogens in its capacity to produce the virulence factor phenolic glycolipid (PGL)-I. In addition to mediating bacterial tropism for neurons, PGL-I interacts with Complement Receptor (CR)3 on macrophages (MPs) to promote infection. We demonstrate here that PGL-I binding to CR3 also enhances bacterial invasion of both polymorphonuclear neutrophils (PMNs) and dendritic cells (DCs). Moreover, in all cell types CR3 engagement by PGL-I activates the Syk tyrosine kinase, inducing calcineurin-dependent nuclear translocation of the transcription factor NFATc. This selectively augments the production of IL-2 by DCs, IL-10 by PMNs and IL-1β by MPs. In intranasally-infected mice PGL-I binding to CR3 heightens mycobacterial phagocytosis by lung PMNs and MPs, and stimulates NFATc-controlled production of Syk-dependent cytokines. Our study thus identifies the CR3-Syk-NFATc axis as a novel signaling pathway activated by PGL-I in innate immune cells, rewiring host cytokine responses to .

https://www.ncbi.nlm.nih.gov/pubmed/31921172