RESEARCH ARTICLE


Basophil Functions During Type 2 Inflammation: Initiators, Regulators and Effectors



Mark C. Siracusa, David Artis*
Department of Pathobiology, University of Pennsylvania, Philadelphia, Pennsylvania, USA

Article Information


Identifiers and Pagination:

Year: 2010
Volume: 3
First Page: 46
Last Page: 51
Publisher Id: TOALLJ-3-46
DOI: 10.2174/1874838401003010046

Article History:

Received Date: 12/3/2010
Revision Received Date: 16/4/2010
Acceptance Date: 7/5/2010
Electronic publication date: 26/11/2010
Collection year: 2010

© 2010 Siracusa and Artis;

open-access license: This is an open access article distributed under the terms of the Creative Commons Attribution 4.0 International Public License (CC-BY 4.0), a copy of which is available at: https://creativecommons.org/licenses/by/4.0/legalcode. This license permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

* Address correspondence to this author at the Department of Microbiology and Department of Pathobiology, University of Pennsylvania, 314 Hill Pavilion, 380 S University Avenue, Philadelphia, Pennsylvania 19104, USA; Tel: 215-898-7920; Fax: 215-746-2295; E-mail: dartis@vet.upenn.edu


Abstract

Recent studies have identified several previously unrecognized functions of basophils in multiple models of Th2 cytokine-dependent immunity and inflammation. In addition to their established role as effector cells in inflamed tissues, findings now indicate that basophils express MHC class II and co-stimulatory molecules, can migrate into draining lymph nodes, present antigen to naive CD4+ T cells and promote Th2 cell differentiation. In this context, basophils have been shown to be critically important for the induction and propagation of Th2 cytokine responses following exposure to helminth parasites and allergens. This article reviews recent conceptual advances in our understanding of basophil biology in the context of allergy and helminth infection.

Keywords: Basophil, Th2 cells, allergic inflammation.