Synergistic cooperation and crosstalk between MYD88^L265P and mutations that dysregulate CD79B and surface IgM.

ABSTRACT: CD79B and MYD88 mutations are frequently and simultaneously detected in B cell malignancies. It is not known if these mutations cooperate or how crosstalk occurs. Here we analyze the consequences of CD79B and MYD88^L265P mutations individually and combined in normal activated mouse B lymphocytes. CD79B mutations alone increased surface IgM but did not enhance B cell survival, proliferation, or altered NF-κB responsive markers. Conversely, B cells expressing MYD88^L265P decreased surface IgM coupled with accumulation of endoglycosidase H-sensitive IgM intracellularly, resembling the trafficking block in anergic B cells repeatedly stimulated by self-antigen. Mutation or overexpression of CD79B counteracted the effect of MYD88

SUBMITTER: Wang JQ 

PROVIDER: S-EPMC5584117 | biostudies-literature | 2017 Sep

REPOSITORIES: biostudies-literature