CD20: Difference between revisions
CSV import Tag: Reverted |
No edit summary Tag: Manual revert |
||
| Line 36: | Line 36: | ||
{{medicine-stub}} | {{medicine-stub}} | ||
{{No image}} | {{No image}} | ||
Latest revision as of 18:24, 18 March 2025
CD20 is a protein that is encoded by the MS4A1 gene in humans. It is a B-lymphocyte surface molecule involved in the development and differentiation of B-cells into plasma cells. CD20 is widely used as a target for the treatment of B-cell lymphomas and leukemias.
Structure[edit]
CD20 is a non-glycosylated phosphoprotein with a molecular weight of approximately 33-37 kDa. It spans the cell membrane four times, creating two extracellular loops, one intracellular loop, and both the N- and C-termini are located within the cytoplasm.
Function[edit]
CD20 plays a crucial role in the regulation of B-cell activation and proliferation. It is involved in the transmembrane calcium channel activity, which is essential for B-cell receptor (BCR) signaling. The exact mechanism of CD20 function is not fully understood, but it is known to be important for the optimal immune response.
Clinical Significance[edit]
CD20 is an important target in the treatment of B-cell malignancies. Monoclonal antibodies such as rituximab, ofatumumab, and obinutuzumab target CD20 and are used in the treatment of diseases like non-Hodgkin lymphoma, chronic lymphocytic leukemia, and rheumatoid arthritis. These therapies work by binding to CD20 on the surface of B-cells, leading to cell death through mechanisms such as antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and direct induction of apoptosis.
Research[edit]
Ongoing research is focused on understanding the precise role of CD20 in B-cell physiology and its potential as a therapeutic target. Studies are also exploring the development of new CD20-targeting agents and combination therapies to improve treatment outcomes for patients with B-cell malignancies.
Related Pages[edit]
References[edit]
<references group="" responsive="1"></references>
External Links[edit]
