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Review
. 2010 Aug;10(8):829-36.
doi: 10.1016/j.intimp.2010.04.014. Epub 2010 Apr 27.

Janus kinase-3 dependent inflammatory responses in allergic asthma

Rama Malaviya  1 , Debra L Laskin, Ravi Malaviya
Affiliations
Review

Janus kinase-3 dependent inflammatory responses in allergic asthma

Rama Malaviya et al. Int Immunopharmacol. 2010 Aug.

Abstract

Allergic asthma is a chronic inflammatory condition of the lung characterized by reversible airway obstruction, high serum immunoglobulin (Ig) E levels, and chronic airway inflammation. A number of cells including mast cells, T cells, macrophages and dendritic cells play a role in the pathogenesis of the disease. Janus kinase (JAK)-3, a non-receptor protein tyrosine kinase, traditionally known to mediate cytokine signaling, also regulates functional responses of these cells. In this review the role of JAK-3 in regulating various pathogenic processes in allergic asthma is discussed. We propose that targeting JAK-3 is a rationale approach to control the inflammatory responses of multiple cell types responsible for the pathogenesis of allergic asthma.

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Figures

Fig. 1
Fig. 1. The JAK-STAT signaling pathway
Upon binding ligand, receptor-associated JAKs become activated and mediate phosphorylation of specific receptor tyrosine residues. This leads to the recruitment of specific STATs, which are then tyrosine-phosphorylated. Activated STATs dimerize, translocate to the nucleus, and bind to members of the γ-activated site family of enhancers.
Fig. 2
Fig. 2. JAK-3 mediated biochemical events
In both hematopoietic and nonhematopoietic cells JAK-3 mediates diverse biochemical responses important in the pathophysiology of allergic asthma. Inflammatory mediators and cytokines released following JAK-3 activation by one cell may influence the responses of neighboring cell types (shown by dashed arrows). Thus, targeting Jak-3 may permit control of functional activation of multiple cell types important in pathogenesis of allergic disease.
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