期刊
MOLECULAR IMMUNOLOGY
卷 89, 期 -, 页码 73-83出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.molimm.2017.05.025
关键词
Complement C1q; Autoimmunity; Pregnancy; Wound healing; Tumor; Neurobiology
资金
- French National Research Agency [ANR-09-PIRI-0021, ANR-16-CE11-0019-01]
- NIH [AG00536]
- NIH NIAID [1R15AI117474]
- Agence Nationale de la Recherche (ANR) [ANR-09-PIRI-0021] Funding Source: Agence Nationale de la Recherche (ANR)
Originally discovered as part of C1, the initiation component of the classical complement pathway, it is now appreciated that C1q regulates a variety of cellular processes independent of complement activation. C1q is a complex glycoprotein assembled from 18 polypeptide chains, with a C-terminal globular head region that mediates recognition of diverse molecular structures, and an N-terminal collagen-like tail that mediates immune effector mechanisms. C1q mediates a variety of immunoregulatory functions considered important in the prevention of autoimmunity such as the enhancement of phagocytosis, regulation of cytokine production by antigen presenting cells, and subsequent alteration in T-lymphocyte maturation. Furthermore, recent advances indicate additional roles for C1q in diverse physiologic and pathologic processes including pregnancy, tissue repair, and cancer. Finally, C1q is emerging as a critical component of neuronal network refinement and homeostatic regulation within the central nervous system. This review summarizes the classical functions of C1q and reviews novel discoveries within the field.
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