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An anti-inflammatory function for the complement anaphylatoxin C5a-binding protein, C5L2.

C5L2 is an enigmatic serpentine receptor that is co-expressed with the C5a receptor on many cells including polymorphonuclear neutrophils. The apparent absence of coupling of C5L2 with G proteins suggests that this receptor may modulate the biological activity of C5a, perhaps by acting as a decoy receptor. Alternatively, C5L2 may affect C5a function through formation of a heteromeric complex with the C5aR, or it may utilize a G protein-independent signaling pathway. Here we show that in mice bearing a targeted deletion of C5L2, the biological activity of C5a/C5a(desArg) is enhanced both in vivo and in vitro. The biological role of C5L2 thus appears to be limiting to the pro-inflammatory response to the anaphylatoxin. Accordingly, up-regulation of C5L2 may be of benefit in inflammatory states driven by C5a, including sepsis, asthma, cystic fibrosis, and chronic obstructive lung disease.

Pubmed ID: 16204243

Authors

  • Gerard NP
  • Lu B
  • Liu P
  • Craig S
  • Fujiwara Y
  • Okinaga S
  • Gerard C

Journal

The Journal of biological chemistry

Publication Data

December 2, 2005

Associated Grants

  • Agency: NHLBI NIH HHS, Id: HL36162
  • Agency: NHLBI NIH HHS, Id: HL69511

Mesh Terms

  • Anaphylatoxins
  • Animals
  • Anti-Inflammatory Agents
  • Bone Marrow Cells
  • Chemotaxis
  • Cloning, Molecular
  • Complement C5a
  • DNA, Complementary
  • Female
  • GTP-Binding Proteins
  • Gene Expression Regulation
  • Inflammation
  • Interleukin-6
  • Lung
  • Lung Injury
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Transgenic
  • Models, Genetic
  • Neutrophils
  • Phenotype
  • Protein Binding
  • RNA, Messenger
  • Receptors, Chemokine
  • Recombinant Proteins
  • Tumor Necrosis Factor-alpha
  • Up-Regulation