TY - JOUR
T1 - Regulation and function of anaphylatoxins and their receptors in allergic asthma
AU - Laumonnier, Yves
AU - Wiese, Anna V.
AU - Figge, Julia
AU - Karsten, Christian
N1 - Funding Information:
This work supported by the Deutsche Forschungsgemeinschaft (DFG) grants RTG 1727 project A5 to C.M.K., and IRTG1911 projects A1and B2 to Y.L. and C.M.K.
Publisher Copyright:
© 2016 Elsevier Ltd
Copyright:
Copyright 2017 Elsevier B.V., All rights reserved.
PY - 2017/4/1
Y1 - 2017/4/1
N2 - Allergic asthma is a disease of the airways driven by maladaptive T helper 2 (Th2) and Th17 immune response against harmless, airborne substances. The hallmarks of this disease are airway hyperresponsiveness (AHR), eosinophilic and neutrophilic airway inflammation and mucus overproduction. Distinct dendric cell (DC) subsets together with airway epithelial and pulmonary vascular endothelial cells play critical roles in allergen sensing and in driving T cell differentiation towards Th2 and Th17 effector or regulatory T cells (Treg). Previous studies suggested already a pivotal role for the anaphylatoxins (C5a, C3a) in the pathogenesis of allergic asthma. During sensitization for example it is described, that C3a promotes, whereas C5a protects from the development of maladaptive immunity during allergen sensitization. Here we will discuss the role of the anaphylatoxins (C3a, C5a) and their receptors during the pathogenesis of allergic asthma, and specifically in lung DC biology. We will also have a look on canonical and non-canonical complement activation and we will discuss novel concepts on how the adaptive immune system can regulate the function of ATRs also in the context of allergic asthma.
AB - Allergic asthma is a disease of the airways driven by maladaptive T helper 2 (Th2) and Th17 immune response against harmless, airborne substances. The hallmarks of this disease are airway hyperresponsiveness (AHR), eosinophilic and neutrophilic airway inflammation and mucus overproduction. Distinct dendric cell (DC) subsets together with airway epithelial and pulmonary vascular endothelial cells play critical roles in allergen sensing and in driving T cell differentiation towards Th2 and Th17 effector or regulatory T cells (Treg). Previous studies suggested already a pivotal role for the anaphylatoxins (C5a, C3a) in the pathogenesis of allergic asthma. During sensitization for example it is described, that C3a promotes, whereas C5a protects from the development of maladaptive immunity during allergen sensitization. Here we will discuss the role of the anaphylatoxins (C3a, C5a) and their receptors during the pathogenesis of allergic asthma, and specifically in lung DC biology. We will also have a look on canonical and non-canonical complement activation and we will discuss novel concepts on how the adaptive immune system can regulate the function of ATRs also in the context of allergic asthma.
UR - http://www.scopus.com/inward/record.url?scp=85007471004&partnerID=8YFLogxK
U2 - 10.1016/j.molimm.2016.11.013
DO - 10.1016/j.molimm.2016.11.013
M3 - Journal articles
C2 - 27916272
AN - SCOPUS:85007471004
SN - 0161-5890
VL - 84
SP - 51
EP - 56
JO - Molecular Immunology
JF - Molecular Immunology
ER -
