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Immunol Res. 2015 Dec;63(1-3):101-6. doi: 10.1007/s12026-015-8705-6.

Fundamental role of C1q in autoimmunity and inflammation.

Author information

1
Center for Autoimmune and Musculoskeletal Diseases, The Feinstein Institute for Medical Research, 350 Community Drive, Manhasset, NY, 11030, USA.
2
Center for Autoimmune and Musculoskeletal Diseases, The Feinstein Institute for Medical Research, 350 Community Drive, Manhasset, NY, 11030, USA. bdiamond@nshs.edu.

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.

KEYWORDS:

Autoimmunity; C1q; Complement; Inflammation; SLE

PMID:
26410546
PMCID:
PMC4894527
DOI:
10.1007/s12026-015-8705-6
[Indexed for MEDLINE]
Free PMC Article

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