Chemokines and Their Receptors as a Target for the Treatment of Contact Hypersensitivity

ISSN: 1875-614X (Online)
ISSN: 1871-5230 (Print)

Volume 16, 3 Issues, 2017

Download PDF Flyer

Anti-Inflammatory & Anti-Allergy Agents in Medicinal Chemistry

Formerly: Current Medicinal Chemistry - Anti-Inflammatory and Anti-Allergy Agents

This journal supports open access

Aims & ScopeAbstracted/Indexed in

Submit Abstracts Online Submit Manuscripts Online

Claudiu T. Supuran
Neurofarba Department
University of Florence

View Full Editorial Board

Subscribe Purchase Articles Order Reprints

Chemokines and Their Receptors as a Target for the Treatment of Contact Hypersensitivity

Anti-Inflammatory & Anti-Allergy Agents in Medicinal Chemistry, 7(1): 45-51.

Author(s): Yoshimi Niwano, Gaku Mitsui and Masahiro Kohno.

Affiliation: Research Center for Functional Food Materials, Sunny Health Holdings Co., Ltd., Saito Biotechnology Incubator, 7-7-15 Saito-Asagi, Ibaragi, Osaka 567-0085, Japan.


Contact hypersensitivity (CHS) is an antigen-specific response elicited by exposure to certain low-molecularweight compounds termed haptens, and is the disease often seen clinically. CHS has also been used as a useful model to assess antigen-specific and T cell-dependent immune response. A wide variety of cells are thought to be involved in the pathogenesis of CHS. Keratinocytes and T cells are regarded as important factors, and besides these cells, mast cells, fibroblasts, B cells, macrophages, neutrophils have been demonstrated to be involved. From the studies of gene knockout experiments, it has been gleaned that IL-1β, IL-2, IL-3, IL-4, IL-6, IL-10, IFN-γ, TNF-α are associated with elicitation of CHS. While the roles of these cytokines in CHS have been well elucidated, recent attention has been directed at members of the superfamily of chemoattractant cytokines that are collectively termed chemokines. Both of mouse and human CHS studies showed chemokine genes were sequentially expressed in the elicitation site, suggesting that chemokine-mediated nonimmunological mechanisms precede and corroborate antigen-specific mechanisms during elicitation of CHS. In a mouse CHS study, topical treatment with a corticosteroid drug suppressed completely the infiltrates as well as the ear swelling response. In addition, the up-regulation of gene expressions for chemokines was suppressed by the corticosteroid drug, indicating that the expression of chemokine genes seems to be essential for orientating non-specific skin response to hapten-specific CHS response through the recruitment of inflammatory cells from the circulation into the tissue site. In this review, we discuss the proposed function of chemokines in the pathogenesis of CHS.


Chemokine, contact hypersensitivity, corticosteroid.

Download Free Order Reprints Order Eprints Rights and Permissions

Article Details

Volume: 7
Issue Number: 1
First Page: 45
Last Page: 51
Page Count: 7
DOI: 10.2174/187152308783769159

Related Journals

Webmaster Contact: Copyright © 2016 Bentham Science