C3a (complement): Difference between revisions
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{{DISPLAYTITLE:C3a (complement)}} | |||
== | == Overview == | ||
C3a is a small protein fragment | [[File:Complement_pathway.svg|thumb|right|Diagram of the complement pathway, illustrating the role of C3a.]] | ||
C3a is a small protein fragment released from the cleavage of the complement component [[C3 (complement)|C3]] during the activation of the [[complement system]]. It is an important part of the body's innate immune response, playing a crucial role in inflammation and defense against pathogens. | |||
==Function== | == Structure and Function == | ||
C3a | C3a is generated when the C3 convertase enzyme cleaves C3 into C3a and [[C3b (complement)|C3b]]. C3a is a potent [[anaphylatoxin]], which means it can induce rapid degranulation of [[mast cells]] and [[basophils]], leading to the release of [[histamine]] and other inflammatory mediators. | ||
== | === Role in Inflammation === | ||
C3a acts as a [[chemoattractant]], recruiting [[neutrophils]] and other immune cells to the site of infection or injury. It also enhances the permeability of blood vessels, allowing immune cells to access affected tissues more easily. This contributes to the classic signs of inflammation: redness, heat, swelling, and pain. | |||
== | === Interaction with Receptors === | ||
C3a exerts its effects by binding to the [[C3a receptor]] (C3aR), a G protein-coupled receptor expressed on various cell types, including [[endothelial cells]], [[smooth muscle cells]], and [[macrophages]]. Activation of C3aR triggers intracellular signaling pathways that mediate the inflammatory response. | |||
== Clinical Significance == | |||
[[File:Complement_pathway.svg|thumb|left|The complement pathway, highlighting the activation of C3a.]] | |||
Dysregulation of C3a activity is implicated in several pathological conditions. Excessive C3a production can contribute to chronic inflammatory diseases such as [[asthma]], [[rheumatoid arthritis]], and [[systemic lupus erythematosus]]. Conversely, inadequate C3a activity may impair the immune response, increasing susceptibility to infections. | |||
== Related Pages == | |||
* [[Complement system]] | * [[Complement system]] | ||
* [[C3 (complement)]] | |||
* [[C3b (complement)]] | |||
* [[Anaphylatoxin]] | |||
* [[C3a receptor]] | * [[C3a receptor]] | ||
[[Category:Immunology]] | |||
[[Category:Complement system]] | |||
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Latest revision as of 11:12, 15 February 2025
Overview[edit]

C3a is a small protein fragment released from the cleavage of the complement component C3 during the activation of the complement system. It is an important part of the body's innate immune response, playing a crucial role in inflammation and defense against pathogens.
Structure and Function[edit]
C3a is generated when the C3 convertase enzyme cleaves C3 into C3a and C3b. C3a is a potent anaphylatoxin, which means it can induce rapid degranulation of mast cells and basophils, leading to the release of histamine and other inflammatory mediators.
Role in Inflammation[edit]
C3a acts as a chemoattractant, recruiting neutrophils and other immune cells to the site of infection or injury. It also enhances the permeability of blood vessels, allowing immune cells to access affected tissues more easily. This contributes to the classic signs of inflammation: redness, heat, swelling, and pain.
Interaction with Receptors[edit]
C3a exerts its effects by binding to the C3a receptor (C3aR), a G protein-coupled receptor expressed on various cell types, including endothelial cells, smooth muscle cells, and macrophages. Activation of C3aR triggers intracellular signaling pathways that mediate the inflammatory response.
Clinical Significance[edit]

Dysregulation of C3a activity is implicated in several pathological conditions. Excessive C3a production can contribute to chronic inflammatory diseases such as asthma, rheumatoid arthritis, and systemic lupus erythematosus. Conversely, inadequate C3a activity may impair the immune response, increasing susceptibility to infections.