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Basophils as key regulators of allergic inflammation and Th2-type immunity

Gibbs, Bernhard F (2008) Basophils as key regulators of allergic inflammation and Th2-type immunity. World Allergy Organization Journal, 1 (7). pp. 123-128. (doi:10.1097/WOX.0b013e31817a76fb) (The full text of this publication is not currently available from this repository. You may be able to access a copy if URLs are provided) (KAR id:4788)

The full text of this publication is not currently available from this repository. You may be able to access a copy if URLs are provided.
Official URL:
http://dx.doi.org/10.1097/WOX.0b013e31817a76fb

Abstract

Basophils have long been suspected as playing more than a bystander role in initiating and maintaining allergic disorders, despite their relatively low numbers compared with other effector cells, such as mast cells and eosinophils. In vitro studies clearly demonstrated their propensity to generate proallergic cytokines, such as interleukin 4 and interleukin 13, as well as histamine and leukotrienes after simulation with allergens and innate IgE-dependent triggers. However, only very recently have mouse basophils been identified as key regulators of allergy in vivo, including orchestrating Th2 immunity to protease allergens in the induction phase. This review highlights these exciting advances that go far in unraveling our understanding of basophil function in the orchestration of allergic inflammation.

Item Type: Article
DOI/Identification number: 10.1097/WOX.0b013e31817a76fb
Additional information: Review article.
Uncontrolled keywords: basophils; mast cells; Th2 immunity; allergy
Subjects: R Medicine
Q Science > QR Microbiology > QR180 Immunology
Divisions: Divisions > Division of Natural Sciences > Medway School of Pharmacy
Depositing User: Bernhard F. Gibbs
Date Deposited: 29 Jun 2011 12:13 UTC
Last Modified: 16 Nov 2021 09:43 UTC
Resource URI: https://kar.kent.ac.uk/id/eprint/4788 (The current URI for this page, for reference purposes)

University of Kent Author Information

Gibbs, Bernhard F.

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