Institutional members access full text with Ovid®

Share this article on:

The role of eosinophils and basophils in allergic diseases considering genetic findings

Nadif, Rachel; Zerimech, Farid; Bouzigon, Emmanuelle; Matran, Regis

Current Opinion in Allergy & Clinical Immunology: October 2013 - Volume 13 - Issue 5 - p 507–513
doi: 10.1097/ACI.0b013e328364e9c0
GENETICS AND EPIDEMIOLOGY: Edited by Catherine Laprise and Emmanuelle Bouzigon

Purpose of review: Basophils and eosinophils represent less than 1 and 5% of white blood cells, respectively. Their role in asthma and allergic inflammation remains incompletely defined. The present review addresses recent advances regarding the role of these two cell populations in allergic inflammation and asthma regarding both biological and genetic point of view.

Recent findings: Regarding eosinophils, the role of interleukin(IL)-25, IL-33 and thymic stromal lymphoprotein (TSLP) have been evidenced, and activation states of eosinophil β1 and β2 integrins have been found to correlate with the measurement of eosinophil recruitment and pulmonary function in asthma. New insights into the biology of basophils concern their role as regulators of Th2 cell response through IL-4 expression or the differentiation of monocytes to macrophages, and their population heterogeneity in human. The transcription factor PU.1 was reported to be involved in controlling transcription of specific genes both in eosinophils and basophils. Candidate genetic studies on eosinophils have explored genes involved in the intracellular calcium influx and apoptosis. At the genome-wide level, studies identified genetic variants belonging to IL1RL1, TSLP and IL-33, and four loci with pleiotropic effects on eosinophil and basophil counts [GATA2 (3q21), MHC (6p21), HBS1L-MYB (6q23), and ERG (21q22)].

Summary: Recent findings from biological and genetic studies on eosinophils and basophils highlight the role of epithelial cell-derived cytokines such as TSLP and IL-33 in asthma and allergic diseases.

aInserm, Centre for research in Epidemiology and Population Health (CESP), U1018, Respiratory and Environmental Epidemiology Team

bUniv Paris-Sud, UMRS 1018, Villejuif

cCHRU de Lille

dUniv Lille Nord de France, Lille

eUniv Paris Diderot, Sorbonne Paris Cité, Institut Universitaire d’Hématologie

fInserm, UMR-946, F-75010, Paris, France

Correspondence to Rachel Nadif, PhD, Inserm, Centre for research in Epidemiology and Population Health (CESP), U1018, Respiratory and Environmental Epidemiology Team, F-94807 Villejuif, France. Tel: +33 0 145 59 51 89; fax: +33 0 145 59 51 69; e-mail: rachel.nadif@inserm.fr

Copyright © 2013 Wolters Kluwer Health, Inc. All rights reserved.