A complex role for complement in allergic asthma
Xun Zhang, Jörg Köhl, Xun Zhang, Jörg Köhl
Abstract
Allergic asthma is a chronic inflammatory disease of the upper airway. It is well appreciated that maladaptive Th2 immunity promotes the allergic phenotype, the underlying mechanisms of which remain elusive. The disease is associated with activation of complement, an ancient danger-sensing component of the innate immune system. Different models of experimental allergic asthma suggest that the small complement fragments of C3 and C5, the anaphylatoxins C3a and C5a, not only promote proallergic effector functions during the allergic effector phase but regulate the development of Th2 immunity during allergen sensitization. The available data support a concept in which C5a is dominant during allergen sensitization and protects against the development of maladaptive Th2 immunity. By contrast, C3a and C5a appear to act synergistically and drive allergic inflammation during the effector phase. In this article, we will review the recent findings in the field to judge the benefit of complement targeting in allergic asthma.
Keywords: Th2 cytokine; allergic asthma; anaphylatoxin; complement; dendritic cell; innate immunity.
Conflict of interest statement
Financial & competing interests disclosure
This work has been supported by NIH grant AI057839 and DFG Transregio 22 project A21 to Jörg Köhl. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.
No writing assistance was utilized in the production of this manuscript.
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Source: PubMed