CD3-epsilon overexpressed in prothymocytes acts as an oncogene.

Background Upon engagement of the T cell receptor for antigen, its associated CD3 proteins recruit signal transduction molecules, which in turn regulate T lymphocyte proliferation, apoptosis, and thymocyte development. Because some signal transducing molecules recruited by CD3-e, i.e., p56lck and p59fyn, are oncogenic and since we previously found that overexpression of CD3-e transgenes causes a block in T lymphocyte and NK cell development, we tested the hypothesis that aberrant CD3-e signaling leads both to abnormal T lymphocyte death and lymphomagenesis.