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Going through Changes: Surface IgM Levels during CLL Therapy with Ibrutinib
1Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas. jaburger@mdanderson.org.
Continuous B-cell receptor (BCR) stimulation by antigens in secondary lymphoid tissues is a key pathogenic mechanism in chronic lymphocytic leukemia (CLL). Therapy with ibrutinib mobilizes tissue CLL cells into the peripheral blood (PB), away from tissue antigen. Consequently, mobilized antigen-deprived CLL cells upregulate surface immunoglobulin M (IgM), providing robust evidence for this mechanism of pathogenesis.See related article by Drennan et al., p. 2503.
Continuous B-cell receptor (BCR) stimulation by antigens in secondary lymphoid tissues is a key pathogenic mechanism in chronic lymphocytic leukemia (CLL). Therapy with ibrutinib mobilizes tissue CLL cells into the peripheral blood (PB), away from tissue antigen. Consequently, mobilized antigen-deprived CLL cells upregulate surface immunoglobulin M (IgM), providing robust evidence for this mechanism of pathogenesis.See related article by Drennan et al., p. 2503.
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