Jun 29, 2017

Allergic airway inflammation: key players beyond the Th2 cell pathway

Immunological Reviews
Koichi HiroseHiroshi Nakajima

Abstract

Allergic asthma is characterized by eosinophilic airway inflammation, mucus hyperproduction, and airway hyperreactivity, causing reversible airway obstruction. Accumulating evidence indicates that antigen-specific Th2 cells and their cytokines such as IL-4, IL-5, and IL-13 orchestrate these pathognomonic features of asthma. However, over the past decade, the understanding of asthma pathogenesis has made a significant shift from a Th2 cell-dependent, IgE-mediated disease to a more complicated heterogeneous disease. Recent studies clearly show that not only Th2 cytokines but also other T cell-related cytokines such as IL-17A and IL-22 as well as epithelial cell cytokines such as IL-25, IL-33, and thymic stromal lymphopoietin (TSLP) are involved in the pathogenesis of asthma. In this review, we focus on the roles of these players beyond Th2 pathways in the pathogenesis of asthma.

  • References225
  • Citations38

Citations

Mentioned in this Paper

TSLP protein, human
Eosinophil
Study
Pathogenic Aspects
Biochemical Pathway
C19orf10 gene
T-Lymphocyte
Pathogenesis
Immediate Hypersensitivity
Interleukin-1

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