The regulation of the complement system: insights from genetically-engineered mice

Turnberg, Daniel

doi:10.1016/s0161-5890(03)00110-x

Cited by 53 publications

(46 citation statements)

References 100 publications

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“…To prevent nonspecific C3b degradation, for instance in the case of proper complement activation, Factor I requires cofactors for its proteolytic activity. These cofactors include membrane cofactor protein (MCP; CD46), complement receptor 1 (CR1), and Factor H which are either intrinsic membrane proteins on host cells or have various mechanisms to ensure preferential cofactor activity on host surfaces, and thereby limit complement activation in these contexts and prevent bystander tissue damage [38][39][40].…”

Section: Regulation Of Complement Activationmentioning

confidence: 99%

Complement and its role in innate and adaptive immune responses

2009

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The complement system plays a crucial role in the innate defense against common pathogens. Activation of complement leads to robust and efficient proteolytic cascades, which terminate in opsonization and lysis of the pathogen as well as in the generation of the classical inflammatory response through the production of potent proinflammatory molecules. More recently, however, the role of complement in the immune response has been expanded due to observations that link complement activation to adaptive immune responses. It is now appreciated that complement is a functional bridge between innate and adaptive immune responses that allows an integrated host defense to pathogenic challenges. As such, a study of its functions allows insight into the molecular underpinnings of host-pathogen interactions as well as the organization and orchestration of the host immune response. This review attempts to summarize the roles that complement plays in both innate and adaptive immune responses and the consequences of these interactions on host defense.

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Section: Regulation Of Complement Activationmentioning

confidence: 99%

Complement and its role in innate and adaptive immune responses

2009

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“…Hence, complement regulators are placed throughout the complement activation cascades (71,84,141), and a number of these are relevant to glomerular diseases (89,107). The human podocyte bears CR1 (57), decay-accelerating factor (DAF; CD55) (110), and CD59 (114).…”

Section: Influence Of Complement Regulatory Proteins In Experimental Mnmentioning

confidence: 99%

Experimental membranous nephropathy redux

Cybulsky

Quigg²,

Salant³

2005

American Journal of Physiology-Renal Physiology

117

133

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Membranous nephropathy (MN) is a common cause of nephrotic syndrome in adults. Active and passive Heymann nephritis (HN) in rats are valuable experimental models because their features so closely resemble human MN. In HN, subepithelial immune deposits form in situ as a result of circulating antibodies. Complement activation leads to assembly of C5b-9 on glomerular epithelial cell (GEC) plasma membranes and is essential for sublethal GEC injury and the onset of proteinuria. This review revisits HN and focuses on areas of substantial progress in recent years. The response of the GEC to sublethal C5b-9 attack is not simply due to disruption of the plasma membrane but is due to the activation of specific signaling pathways. These include activation of protein kinases, phospholipases, cyclooxygenases, transcription factors, growth factors, NADPH oxidase, stress proteins, proteinases, and others. Ultimately, these signals impact on cell metabolic pathways and the structure/function of lipids and key proteins in the cytoskeleton and slit-diaphragm. Some signals affect GEC adversely. Thus C5b-9 induces partial dissolution of the actin cytoskeleton. There is a decline in nephrin expression, reduction in F-actin-bound nephrin, and loss of slit-diaphragm integrity. Other signals, such as endoplasmic reticulum stress, may limit complement-induced injury, or promote recovery. The extent of complement activation and GEC injury is dependent, in part, on complement-regulatory proteins, which act at early or late steps within the complement cascade. Identification of key steps in complement activation, the cellular signaling pathways, and the targets will facilitate therapeutic intervention in reversing GEC injury in human MN.

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“…α-2-Macroglobulin (A2M) may be involved in the pathway of complementation and coagulation cascades to eliminate pathogens (Turnberg and Botto, 2003). The abundance of these two proteins was elevated in the LM of pigs fed NSPEs.…”

Section: Discussionmentioning

confidence: 99%

iTRAQ-based quantitative proteomic analysis of longissimus muscle from growing pigs with dietary supplementation of non-starch polysaccharide enzymes

Zhang

Gao

et al. 2015

J. Zhejiang Univ. Sci. B

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Non-starch polysaccharide enzymes (NSPEs) have long been used in the feed production of monogastric animals to degrade non-starch polysaccharide to oligosaccharides and promote growth performance. However, few studies have been conducted on the effect of such enzymes on skeletal muscle in monogastric animals. To elucidate the mechanism of the effect of NSPEs on skeletal muscle, an isobaric tag for relative and absolute quantification (iTRAQ) for differential proteomic quantitation was applied to investigate alterations in the proteome in the longissimus muscle (LM) of growing pigs after a 50-d period of supplementation with 0.6% NSPEs in the diet. A total of 51 proteins were found to be differentially expressed in the LM between a control group and the NSPE group. Functional analysis of the differentially expressed protein species showed an increased abundance of proteins related to energy production, protein synthesis, muscular differentiation, immunity, oxidation resistance and detoxification, and a decreased abundance of proteins related to inflammation in the LM of the pigs fed NSPEs. These findings have important implications for understanding the mechanisms whereby dietary supplementation with NSPEs enzymes can promote growth performance and improve muscular metabolism in growing pigs.

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The regulation of the complement system: insights from genetically-engineered mice

Cited by 53 publications

References 100 publications

Complement and its role in innate and adaptive immune responses

Complement and its role in innate and adaptive immune responses

Experimental membranous nephropathy redux

iTRAQ-based quantitative proteomic analysis of longissimus muscle from growing pigs with dietary supplementation of non-starch polysaccharide enzymes

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