C5L2 is critical for the biological activities of the anaphylatoxins C5a and C3a

Nien Jung Chen, Christine Mirtsos, Daniel Suh, Yong Chen Lu, Wen Jye Lin, Colin McKerlie, Taeweon Lee, Helene Baribault, Hui Tian, Wen Chen Yeh*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

198 Scopus citations


Complement-derived anaphylatoxins regulate immune and inflammatory responses through G-protein-coupled receptor (GPCR)-mediated signalling. C5L2 (also known as GPR77) is a relatively new GPCR thought to be a non-signalling receptor binding to C5a, on the basis of sequence information and experimental evidence. Here we show, using gene targeting, that C5L2 is required to facilitate C5a signalling in neutrophils, macrophages and fibroblasts in vitro. Deficiency of C5L2 results in reduced inflammatory cell infiltration, suggesting that C5L2 is critical for optimal C5a-mediated cell infiltration in certain in vivo settings. C5L2 is also involved in optimizing C3a-induced signals. Furthermore, like mice incapable of C3a/complement 3a receptor (C3aR) signalling, C5L2-deficient mice are hypersensitive to lipopolysaccharide (LPS)-induced septic shock, show reduced ovalbumin (OVA)-induced airway hyper-responsiveness and inflammation, and are mildly delayed in haematopoietic cell regeneration after γ-irradiation. Our data indicate that C5L2 can function as a positive modulator for both C5a- and C3a-anaphylatoxin-induced responses.

Original languageEnglish
Pages (from-to)203-207
Number of pages5
Issue number7132
StatePublished - 8 Mar 2007


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