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 and Wen-Chen Yeh ()
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Nien-Jung Chen: The Campbell Family Institute for Breast Cancer Research, Ontario Cancer Institute, University of Toronto, Toronto, Ontario M5G 2C1, Canada
Christine Mirtsos: The Campbell Family Institute for Breast Cancer Research, Ontario Cancer Institute, University of Toronto, Toronto, Ontario M5G 2C1, Canada
Daniel Suh: The Campbell Family Institute for Breast Cancer Research, Ontario Cancer Institute, University of Toronto, Toronto, Ontario M5G 2C1, Canada
Yong-Chen Lu: The Campbell Family Institute for Breast Cancer Research, Ontario Cancer Institute, University of Toronto, Toronto, Ontario M5G 2C1, Canada
Wen-Jye Lin: The Campbell Family Institute for Breast Cancer Research, Ontario Cancer Institute, University of Toronto, Toronto, Ontario M5G 2C1, Canada
Colin McKerlie: Hospital for Sick Children, Toronto, Ontario M5G 1X8, Canada
Taeweon Lee: Amgen San Francisco, 1120 Veterans Boulevard, South San Francisco, California 94080, USA
Helene Baribault: Amgen San Francisco, 1120 Veterans Boulevard, South San Francisco, California 94080, USA
Hui Tian: Amgen San Francisco, 1120 Veterans Boulevard, South San Francisco, California 94080, USA
Wen-Chen Yeh: The Campbell Family Institute for Breast Cancer Research, Ontario Cancer Institute, University of Toronto, Toronto, Ontario M5G 2C1, Canada

Nature, 2007, vol. 446, issue 7132, 203-207

Abstract: Abstract Complement-derived anaphylatoxins regulate immune and inflammatory responses through G-protein-coupled receptor (GPCR)-mediated signalling1,2,3,4. 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 evidence5,6,7. 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) signalling4,8,9, 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.

Date: 2007
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DOI: 10.1038/nature05559

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