Anti-Human CD20 (Rituximab)

CD20 is a nonglycosylated 33-37 kDa transmembrane-spanning phosphoprotein that is a member of the MS4A family which is widely expressed on normal B cell surfaces during all stages of development as well as by most B cell malignancies1, 2.

The biological role of CD20 remains poorly understood; however, it is thought to be involved in calcium ion influx.

CD20 has no natural ligand and is not immediately internalized upon antibody binding.

Thus, mAbs directed against CD20 depend on the recruitment of a host response.

CD20 is a popular target for mAb therapy because depleting developing B-cells generally does not cause permanent side effects (due to the fact that mature plasma cells and B-cell progenitors do not express CD20 and that there is limited expression of CD20 among other cell lineages).

Rituximab is a chimeric monoclonal antibody that binds to CD20.

Rituximab is used to treat some autoimmune diseases and types of cancer such as non-Hodgkin lymphoma, chronic lymphocytic leukemia, and rheumatoid arthritis among others.

The Fc portion of Rituximab mediates antibody-dependent cellular cytotoxicity (ADCC) and complement-dependent cytotoxicity (CDC).

Rituximab increases MHC II and adhesion molecules LFA-1 and LFA-3 (lymphocyte function-associated antigen) and also induces apoptosis of CD20+ cells.

This ultimately results in the elimination of B cells (including the cancerous ones) from the body, and thus allows a new population of healthy B cells to develop from lymphoid stem cells.

Anti-Human CD20 (Rituximab) utilizes the same variable regions from the therapeutic antibody Rituximab making it ideal for research projects.