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Fundamental role of C1q in autoimmunity and inflammation

  • AUTOIMMUNITY/IMMUNOREGULATION/INFLAMMATION
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Abstract

C1q, historically viewed as the initiating component of the classical complement pathway, also exhibits a variety of complement-independent activities in both innate and acquired immunity. Recent studies focusing on C1q’s suppressive role in the immune system have provided new insight into how abnormal C1q expression and bioactivity may contribute to autoimmunity. In particular, molecular networks involving C1q interactions with cell surface receptors and other ligands are emerging as mechanisms involved in C1q’s modulation of immunity. Here, we discuss the role of C1q in controlling immune cell function, including recently elucidated mechanisms of action, and suggest how these processes are critical for maintaining tissue homeostasis under steady-state conditions and in preventing autoimmunity.

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Acknowledgments

We would like to thank H.S. Yoon for discussions and S. Jones for help. This work was supported by a grant from the National Institute of Arthritis and Musculoskeletal and Skin Disease of the National Institutes of Health (K01AR065506-01 for M.S.; R01AR07084 for B.D.).

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  1. Center for Autoimmune and Musculoskeletal Diseases, The Feinstein Institute for Medical Research, 350 Community Drive, Manhasset, NY, 11030, USA

    Myoungsun Son, Betty Diamond & Frances Santiago-Schwarz

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  1. Myoungsun Son
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Correspondence to Betty Diamond.

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Son, M., Diamond, B. & Santiago-Schwarz, F. Fundamental role of C1q in autoimmunity and inflammation. Immunol Res 63, 101–106 (2015). https://doi.org/10.1007/s12026-015-8705-6

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