Extrahepatic complement biosynthesis: where, when and why?

Morgan, B. Paul; Gasque, Philippe

doi:10.1046/j.1365-2249.1997.d01-890.x

Cited by 310 publications

(232 citation statements)

References 36 publications

(47 reference statements)

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“…Additionally, C2 and C4, which are also part of the CP, have been shown to be secreted by monocytes [26,28,[57][58][59]. Monocytes also secrete various AP components as C3, FB, FD and FP [24,[59][60][61][62][63][64]. Moreover, the terminal pathway components C5, C6, C7, C8 and C9 are secreted, which are able to assemble as MAC [24,65].…”

Section: Monocytesmentioning

confidence: 99%

“…Other tissues also contain cells capable of complement production; for example, endothelial and epithelial cells are also able to secrete various complement components [24], thereby contributing to local processes (Fig. 2).…”

Section: Introductionmentioning

confidence: 99%

“…2). However, for C1q, FP and factor D (FD) it has been shown that the major/only site of production is outside the liver [24][25][26][27][28][29][30]. Additionally, there is a growing body of evidence that local secretion of complement proteins plays an important role in regulating physiological processes even in the absence of further complement activation.…”

Section: Introductionmentioning

confidence: 99%

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Production of complement components by cells of the immune system

Lubbers

Essen

Kooten

et al. 2017

Clinical and Experimental Immunology

378

281

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SummaryThe complement system is an important part of the innate immune defence. It contributes not only to local inflammation, removal and killing of pathogens, but it also assists in shaping of the adaptive immune response. Besides a role in inflammation, complement is also involved in physiological processes such as waste disposal and developmental programmes. The complement system comprises several soluble and membrane-bound proteins. The bulk of the soluble proteins is produced mainly by the liver. While several complement proteins are produced by a wide variety of cell types, other complement proteins are produced by only a few related cell types. As these data suggest that local production by specific cell types may have specific functions, more detailed studies have been employed recently analysing the local and even intracellular role of these complement proteins.Here we review the current knowledge about extrahepatic production and/ or secretion of complement components. More specifically, we address what is known about complement synthesis by cells of the human immune system.

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Section: Monocytesmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Production of complement components by cells of the immune system

Lubbers

Essen

Kooten

et al. 2017

Clinical and Experimental Immunology

378

281

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“…C3 plays a central role in the complement cascade (15). Hepatocytes are the major source of the circulating or systemic pools of C3, although significant, but smaller, amounts are produced locally by cells of the immune system or by other cell types (23,24). The locally produced complement components contribute to the activation of APCs and T cells and drive CD4 + T cell differentiation, expansion, and survival (25)(26)(27).…”

Section: /2mentioning

confidence: 99%

Systemic C3 Modulates CD8+ T Cell Contraction after Listeria monocytogenes Infection

Tan

et al. 2014

The Journal of Immunology

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Ag-specific CD8+ T cell contraction (contraction), which occurs after the resolution of infection, is critical for homeostasis of the immune system. Although complement components regulate the primary CD8+ T cell response, there is insufficient evidence supporting their role in regulating contraction and memory. In this study, we show that C3-deficient (C3−/−) mice exhibited significantly less CD8+ T cell contraction than did wild-type mice postinfection with recombinant Listeria monocytogenes expressing OVA. Kinetic analyses also revealed decreased contraction in mice treated with cobra venom factor to deplete C3, which was consistent with the results in C3−/− recipient mice transplanted with bone marrow cells from the same donors as wild-type recipient mice. The phenotypes of memory cells generated by C3−/− mice were not altered compared with those of wild-type mice. Further, C5aR signaling downstream of C3 was not involved in the regulation of contraction. Moreover, the regulation of contraction by C3 may be independent of the duration of antigenic stimulation or the functional avidity of effector CD8+ T cells. However, reduced contraction in C3−/− mice was accompanied by a decrease in the proportion of KLRG-1hi (killer-cell lectin-like receptor G1) CD127lo short-lived effector cells at the peak of the response and correlated with a reduction in the levels of inflammatory cytokines, such as IL-12 and IFN-γ, produced early postinfection. These results provide new insights into the role of systemic C3 in regulating contraction following intracellular bacterial infection and may help to develop vaccines that are more effective.

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“…Many other non-hepatic cells including macrophage, endothelial, neutrophil and lymphocytes could produce complement proteins. This local synthesis of complement occurs in the brain, heart, lung, joints, intestine, skeletal muscle and bone marrow (Morgan and Gasque, 1997). It has been demonstrated that the absence of locally synthesized complement component C3 is capable of modulating the rejection of renal allografts in vivo and regulating T-cell responses in vivo and in vitro (Pratt et al, 2002).…”

Section: Complement Activationmentioning

confidence: 99%