Complement component 5a: Difference between revisions
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== Complement Component 5a == | |||
[[File:C5a-3D.png|thumb|right|3D structure of Complement Component 5a]] | |||
C5a is a | Complement Component 5a (C5a) is a potent [[anaphylatoxin]] and a key player in the [[complement system]], which is part of the [[innate immune system]]. C5a is a small protein fragment released from the cleavage of [[complement component 5]] (C5) by the enzyme [[C5 convertase]]. | ||
== | === Structure === | ||
C5a is a 74-amino acid glycoprotein with a molecular weight of approximately 11 kDa. It is characterized by a core structure stabilized by three disulfide bonds. The 3D structure of C5a reveals a compact, globular shape that is crucial for its interaction with its receptor, [[C5a receptor]] (C5aR), on target cells. | |||
C5a | === Function === | ||
C5a plays a critical role in the immune response by acting as a powerful [[chemoattractant]] for [[neutrophils]], [[eosinophils]], [[basophils]], and [[monocytes]]. It promotes the migration of these cells to sites of infection or injury. Additionally, C5a induces the degranulation of [[mast cells]] and [[basophils]], leading to the release of [[histamine]] and other inflammatory mediators. | |||
== | === Receptors === | ||
C5a exerts its effects primarily through binding to the C5a receptor (C5aR), also known as CD88, which is a [[G protein-coupled receptor]] expressed on the surface of various immune cells. Another receptor, C5L2, also binds C5a but its role is less well understood and is thought to act as a decoy receptor. | |||
=== Role in Disease === | |||
C5a is implicated in various inflammatory and autoimmune diseases due to its potent pro-inflammatory effects. Elevated levels of C5a are associated with conditions such as [[sepsis]], [[rheumatoid arthritis]], and [[systemic lupus erythematosus]]. Therapeutic strategies targeting C5a or its receptor are being explored to mitigate excessive inflammation in these diseases. | |||
== | === Regulation === | ||
The activity of C5a is tightly regulated in the body. It is rapidly inactivated by the enzyme [[carboxypeptidase N]], which removes the C-terminal arginine residue, converting C5a into C5a des-Arg, a less active form. | |||
== Related Pages == | |||
* [[Complement system]] | * [[Complement system]] | ||
* [[ | * [[Anaphylatoxin]] | ||
* [[ | * [[C5a receptor]] | ||
* [[ | * [[Innate immune system]] | ||
[[Category:Immunology]] | |||
[[Category:Proteins]] | [[Category:Proteins]] | ||
Latest revision as of 11:00, 15 February 2025
Complement Component 5a[edit]
Complement Component 5a (C5a) is a potent anaphylatoxin and a key player in the complement system, which is part of the innate immune system. C5a is a small protein fragment released from the cleavage of complement component 5 (C5) by the enzyme C5 convertase.
Structure[edit]
C5a is a 74-amino acid glycoprotein with a molecular weight of approximately 11 kDa. It is characterized by a core structure stabilized by three disulfide bonds. The 3D structure of C5a reveals a compact, globular shape that is crucial for its interaction with its receptor, C5a receptor (C5aR), on target cells.
Function[edit]
C5a plays a critical role in the immune response by acting as a powerful chemoattractant for neutrophils, eosinophils, basophils, and monocytes. It promotes the migration of these cells to sites of infection or injury. Additionally, C5a induces the degranulation of mast cells and basophils, leading to the release of histamine and other inflammatory mediators.
Receptors[edit]
C5a exerts its effects primarily through binding to the C5a receptor (C5aR), also known as CD88, which is a G protein-coupled receptor expressed on the surface of various immune cells. Another receptor, C5L2, also binds C5a but its role is less well understood and is thought to act as a decoy receptor.
Role in Disease[edit]
C5a is implicated in various inflammatory and autoimmune diseases due to its potent pro-inflammatory effects. Elevated levels of C5a are associated with conditions such as sepsis, rheumatoid arthritis, and systemic lupus erythematosus. Therapeutic strategies targeting C5a or its receptor are being explored to mitigate excessive inflammation in these diseases.
Regulation[edit]
The activity of C5a is tightly regulated in the body. It is rapidly inactivated by the enzyme carboxypeptidase N, which removes the C-terminal arginine residue, converting C5a into C5a des-Arg, a less active form.
