CD21
CD21, also known as Complement receptor 2 (CR2), is a protein that in humans is encoded by the CR2 gene. CD21 is a receptor for the complement component C3d and is expressed on the surface of B cells, follicular dendritic cells, and some epithelial cells. It plays a crucial role in the immune system by enhancing the ability of B cells to respond to antigens.
Structure[edit | edit source]
CD21 is a type I transmembrane protein that belongs to the family of complement receptors. It is composed of an extracellular domain, a single transmembrane helix, and a short cytoplasmic tail. The extracellular domain contains multiple short consensus repeats (SCRs), which are characteristic of complement control proteins.
Function[edit | edit source]
CD21 functions primarily as a receptor for the complement fragment C3d, which is covalently attached to antigens. When C3d-tagged antigens bind to CD21, it enhances the activation of B cells by lowering the threshold for B cell receptor (BCR) signaling. This process is known as "complement-mediated enhancement of B cell activation."
CD21 also forms part of the B cell co-receptor complex, which includes CD19 and CD81. This complex amplifies the signal received through the BCR, promoting B cell activation, proliferation, and differentiation.
Clinical Significance[edit | edit source]
Alterations in CD21 expression or function can have significant implications for immune function. For example, reduced expression of CD21 has been observed in certain immunodeficiency disorders, such as common variable immunodeficiency (CVID). Additionally, CD21 is exploited by the Epstein-Barr virus (EBV) to infect B cells, as the virus uses CD21 as a receptor to gain entry into the cells.
Research and Therapeutic Implications[edit | edit source]
Understanding the role of CD21 in immune responses has implications for vaccine development and autoimmune disease treatment. Targeting CD21 or its interactions with C3d could potentially modulate immune responses in various clinical settings.
Also see[edit | edit source]
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