The role of TARC in the pathogenesis of allergic asthma

M. Cecilia Berin*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

24 Scopus citations

Abstract

TARC (thymus and activation-regulated chemokine), as a selective chemoattractant of Th2 cells, is a reasonable candidate as a key regulator of Th2-mediated inflammation in allergic asthma. Studies have determined that TARC is up-regulated in the airways of human subjects with asthma and that CCR4- and CCR8-bearing T cells are also present in the airways of asthmatic subjects after allergen challenge. Mouse models of allergic airway inflammation have shown that neutralization of TARC can not only inhibit T-cell and eosinophil infiltration into the lung but can also inhibit bronchial hyperresponsiveness. The exact mechanism by which TARC can participate in allergic inflammation and what triggers the expression of TARC following allergen exposure is still unknown. Studies suggest that it could be involved not only in allergic asthma, but in the pathogenesis of allergic Th2-mediated diseases in general.

Original languageEnglish (US)
Pages (from-to)10-16
Number of pages7
JournalDrug News and Perspectives
Volume15
Issue number1
DOIs
StatePublished - 2002

ASJC Scopus subject areas

  • Drug Discovery
  • Pharmacology

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