Anti-CD20 monoclonal antibodies: beyond B-cells.

Abstract

Anti-CD20 monoclonal antibodies (MoAbs), employed in treating CD20⁺ lymphomas and autoimmune diseases, appear to have broader functions than just eradicating malignant B-cells and decreasing autoantibody production. Rituximab-induced T-cell inactivation, reported both in-vitro and in-vivo, may contribute to the increased risk of T-cell-dependent infections, observed in patients receiving this therapy. T-cell polarization into a suppressive phenotype, often observed in patients receiving rituximab for autoimmune disorders, was reported to be associated with prolonged remissions. Elimination of B-cells serving as antigen-presenting cells, thereby causing impaired T-cell activation, could play a significant role in induction of these changes. Direct binding of rituximab to a CD20dim T-cell population, inducing its depletion, may contribute to the decreased T-cell activation following rituximab therapy. Further investigation of the complex network through which rituximab and new anti-CD20 MoAbs act, would advance the employment of these agents in different clinical settings.

DOI: 10.1016/j.blre.2013.07.002
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@article{Avivi2013AntiCD20MA, title={Anti-CD20 monoclonal antibodies: beyond B-cells.}, author={Irit Avivi and Dina Stroopinsky and Tamar Katz}, journal={Blood reviews}, year={2013}, volume={27 5}, pages={217-23} }