TY - JOUR
T1 - IL-17 and neutrophils: unexpected players in the type 2 immune response.
AU - Allen, Judith E
AU - Sutherland, Tara
AU - Ruckerl, Dominik
N1 - 095831MA, Wellcome Trust, United Kingdom
MR/J001929/1, Medical Research Council, United Kingdom
MR/K01207X/1, Medical Research Council, United Kingdom
Acknowledgements
The authors are supported by funding from the Medical Research Council UK (MR/J001929/1, MR/K01207X/1) and the Wellcome Trust funded Centre for Immunity, Infection and Evolution (095831MA).
PY - 2015/6/1
Y1 - 2015/6/1
N2 - The study of immunity to helminth infection has been central to understanding the function of type 2 cytokines and their targets. Although type 2 cytokines are considered anti-inflammatory and promote tissue repair, they also contribute to allergy and fibrosis. Here, we utilise data from helminth infection models, to illustrate that IL-17 and neutrophils, typically associated with pro-inflammatory responses, are intimately linked with type 2 immunity. Neutrophils work with IL-4Rα-activated macrophages to control incoming larvae but this comes at a cost of enhanced tissue damage. Chitinase like proteins (CLPs) bridge these diverse outcomes, inducing both protective IL-17 and reparative Th2 responses. Dysregulation of CLPs, IL-17 and neutrophils likely contribute to disease severity and pathology associated with type 2 immunity.
AB - The study of immunity to helminth infection has been central to understanding the function of type 2 cytokines and their targets. Although type 2 cytokines are considered anti-inflammatory and promote tissue repair, they also contribute to allergy and fibrosis. Here, we utilise data from helminth infection models, to illustrate that IL-17 and neutrophils, typically associated with pro-inflammatory responses, are intimately linked with type 2 immunity. Neutrophils work with IL-4Rα-activated macrophages to control incoming larvae but this comes at a cost of enhanced tissue damage. Chitinase like proteins (CLPs) bridge these diverse outcomes, inducing both protective IL-17 and reparative Th2 responses. Dysregulation of CLPs, IL-17 and neutrophils likely contribute to disease severity and pathology associated with type 2 immunity.
U2 - 10.1016/j.coi.2015.03.001
DO - 10.1016/j.coi.2015.03.001
M3 - Article
VL - 34
SP - 99
EP - 106
JO - Current Opinion in Immunology
JF - Current Opinion in Immunology
SN - 0952-7915
ER -