Abstract
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.
Highlights
The complement system, an important arm of the innate immune system, is activated in heart failure (HF)
Levels of properdin, the stabilizer of the alternative pathway (AP) C3-convertase, were reduced in HF patients, and similar to factor D (FD), this alteration was marked in patients with NYHA classes III and IV (Fig. 2b)
Levels of terminal C5b-9 complement complex (TCC) were increased in HF patients with NYHA class IV as compared to controls confirming that the complement cascade had been activated to the very end in HF patients with the most advanced clinical disease (Fig. 2d)
Summary
The complement system, an important arm of the innate immune system, is activated in heart failure (HF). We hypothesized that HF patients are characterized by an imbalance of alternative amplification loop components; including properdin and complement factor D and the alternative pathway inhibitor factor H. These components and the activation product, terminal complement complex (TCC), were measured in plasma from 188 HF patients and 67 age- and sex- matched healthy controls by enzyme immunoassay. FH inhibits the formation of the AP convertase by binding to C3-fragments Another important player is complement factor D (FD) which circulates in an active form and cleaves complement factor B (FB) to Ba and Bb6 thereby promoting AP activation (Fig. 1)
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