Matches in SemOpenAlex for { <https://semopenalex.org/work/W3203773975> ?p ?o ?g. }
- W3203773975 endingPage "402" @default.
- W3203773975 startingPage "390" @default.
- W3203773975 abstract "Novel pattern-recognition molecules trigger the complement cascade and, in certain cases, may downregulate components of the system with the goal of evading the host immune response. Genetic and acquired deficiencies of certain complement components are associated with a higher risk of bacterial infections. Extrahepatic complement proteins modulate host defense, especially in the context of intracellular bacteria. Intracellular complement proteins, derived from both biosynthesis and uptake, play critical roles in cellular survival, pathogen burden, and effector function. Structural proteins on the surface of viruses, such as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), contribute to increased complement activation, which is associated with a hyperinflammatory response and worse outcomes. The complement system has historically been entertained as a fluid-phase, hepatically derived system which protects the intravascular space from encapsulated bacteria. However, there has been an increasing appreciation for its role in protection against non-encapsulated pathogens. Specifically, we have an improved understanding of how pathogens are recognized by specific complement proteins, as well as how they trigger and evade them. Additionally, we have an improved understanding of locally derived complement proteins, many of which promote host defense. Moreover, intracellular complement proteins have been identified that facilitate local protection and barrier function despite pathogen invasion. Our review aims to summarize these advances in the field as well as provide an insight into the pathophysiological changes occurring when the system is dysregulated in infection. The complement system has historically been entertained as a fluid-phase, hepatically derived system which protects the intravascular space from encapsulated bacteria. However, there has been an increasing appreciation for its role in protection against non-encapsulated pathogens. Specifically, we have an improved understanding of how pathogens are recognized by specific complement proteins, as well as how they trigger and evade them. Additionally, we have an improved understanding of locally derived complement proteins, many of which promote host defense. Moreover, intracellular complement proteins have been identified that facilitate local protection and barrier function despite pathogen invasion. Our review aims to summarize these advances in the field as well as provide an insight into the pathophysiological changes occurring when the system is dysregulated in infection. a screening assay for testing functional activity of the alternative pathway. acute respiratory distress syndrome, a form of severe acute lung injury that results in impaired oxygen transport from the alveolar space into the blood. autophagy-related 16 like 1 is a protein, encoded by the ATG16L1 gene, which interacts with other proteins and lipids, thus helping it to recognize membranes and activate autophagolysosome formation. cirrhosis-associated immune dysfunction, a condition associated with both increased systemic inflammation and immunodeficiency in patients with end-stage liver disease. a membrane inhibitor of complement that binds to C3b and can also affect intracellular complement signaling. a screening assay for testing functional activity of the classical pathway. cobra venom factor, a reagent used to induce a state of relative C3 deficiency by binding to Factor B, thereby cleaving and consuming C3. an HSP90-like endoplasmic reticulum protein that is involved in the unfolded protein response (UPR). high-mobility group box 1 protein, which binds to RAGE (receptor for advanced glycation end products). intercellular adhesion molecule 1, a transmembrane protein present on endothelial cells and leukocytes. lymphocyte function-associated antigen 1, an integrin present on lymphocytes. membrane-attack complex, or C5b–9, formed upon activation of the complement cascade. mitogen-activated protein kinase. mitochondrial antiviral-signaling protein, located in outer membranes of organelles such as mitochondria; it plays an important role in innate immunity via signal transduction. NOD-, LRR- and pyrin domain-containing protein 3, an intracellular sensor that can detect components of microbes and damaged cells. pattern-recognition molecules are germline-encoded host sensors that can detect pathogen-associated molecular patterns (PAMPs) or damage-associated molecular patterns (DAMPs). pentraxin-3, a component of the pentraxin superfamily that can activate the complement cascade via the classical and lectin pathways. severe acute respiratory syndrome coronavirus 2, the virus responsible for the COVID-19 (coronavirus disease-19) pandemic. thymic stromal lymphoprotein, a cytokine expressed primarily by non-hematopoietic cells that skews naïve T cells to a Th2 phenotype." @default.
- W3203773975 created "2021-10-11" @default.
- W3203773975 creator A5009925807 @default.
- W3203773975 creator A5020960936 @default.
- W3203773975 creator A5039719843 @default.
- W3203773975 creator A5048266715 @default.
- W3203773975 creator A5062598434 @default.
- W3203773975 date "2022-04-01" @default.
- W3203773975 modified "2023-10-15" @default.
- W3203773975 title "Emerging roles of the complement system in host–pathogen interactions" @default.
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