Article

The role of complement in the diagnosis and management of allergic rhinitis and allergic asthma.

Institut für Systemische Entzündungsforschung, Universität zu Lübeck, Ratzeburger Allee 160, 23538, Lübeck, Germany.
Current Allergy and Asthma Reports (Impact Factor: 2.45). 04/2011; 11(2):122-30. DOI: 10.1007/s11882-010-0171-6
Source: PubMed

ABSTRACT Allergic rhinitis and asthma are common chronic inflammatory diseases of the nasal mucus membranes and the upper airways with a high prevalence in Western countries. In addition to maladaptive T-helper type 2 (Th2) immunity, Th17 cells can drive the inflammatory responses in both diseases. Several reports have shown that the complement system is activated locally and systemically in allergic rhinitis and/or allergic asthma patients. Importantly, recent findings in experimental models of allergic rhinitis and allergic asthma suggest that the complement cleavage products complement 3a and complement 5a and the activation of their corresponding receptors in antigen-presenting cells regulate the development of maladaptive Th2 and Th17 immunity. These findings in experimental asthma are corroborated by genome-wide searches and candidate gene studies in humans. We discuss recent findings in experimental and human allergic airway diseases suggesting that complement may serve as a new diagnostic and therapeutic target for both disorders.

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    • "The work on CD46-mediated signals on CD4 + T cells is beginning to give insight into the role of complement in human Th1 induction. A wealth of work establishes also a clear role for complement, and particularly for the anaphylatoxins, in the induction or regulation of Th17, natural regulatory T cell and Th2 responses – however, here, the majority of data in regards to the complement-mediated signalling pathways are currently derived from mouse models [50]. Studies performed in pertinent animal models show that C5a affects the generation and modulation of proinflammatory T cell effector responses of the Th17 type by regulating IL-6 and IL- 1␤ produced by dendritic cells (DCs) and/or macrophages [51]. "
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