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Anaphylatoxins and infectious and non-infectious inflammatory diseases

Kohl J2001Molecular ImmunologyReview
10.1016/s0161-5890(01)00041-4PubMed
CardiovascularImmune/InnateRespiratory/Sinus

Abstract

In recent years a plethora of data has accumulated directing toward an important role of polypeptides C3a and C5a and its degradation product C5adesArg, summarized as anaphylatoxins (ATs), in microbial host defense and immune regulation. The ATs exert their various biologic functions by interacting with specific C3a- and C5a-receptors present on cells of myeloid origin, epithelial cells, smooth muscle cells as well as on activated B- and T-cells. Activation of AT receptors mediates signal transduction pathways triggering a variety of proinflammatory events. However, by interacting with the cytokine- and chemokine network C3a and C5a exhibit also anti-inflammatory properties. In this review the focus is on the pathogenetic role of the ATs in sepsis, immune complex disease, delayed type hypersensitivity and asthma. Discussed are data from animal models in which the ATs are blocked by specific C3a or C5a inhibitors or from mice with genetic deletions of the specific receptors of either C3a or C5a/C5adesArg. © 2001 Elsevier Science Ltd. All rights reserved.

Key Biomarkers

AnaphylatoxinsC3aC3a receptorC5aC5a receptorC5adesArg

Symptom Clusters

AsthmaDelayed type hypersensitivityImmune complex diseaseSepsis

Cited By (11)

  • The role of complement in danger sensing and transmissionImmunologic Research · 2006
  • AnaphylatoxinsImmunologic Research · 2007
  • Pharmacological Targeting of Anaphylatoxin Receptors during the Effector Phase of Allergic Asthma Suppresses Airway Hyperresponsiveness and Airway InflammationThe Journal of Immunology · 2005
  • A regulatory role for the C5a anaphylatoxin in type 2 immunity in asthmaJournal of Clinical Investigation · 2006
  • Inhibition of complement activation decreases airway inflammation and hyperresponsivenessAmerican Journal of Respiratory and Critical Care Medicine · 2003
  • Inhibition of complement and CD14 attenuates the Escherichia coli-induced inflammatory response in porcine whole bloodInfect Immun · 2009
  • Complement regulates inhalation tolerance at the dendritic cell/T cell interfaceMolecular Immunology · 2007

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  • References (5)

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