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The most invasive B-cell lymphoma is often characterized by in-body distribution and carries somatic cell mutations with less obvious characteristics of the TBL1XR1 gene.
recently, researchers have shown that the TBL1XR1 mutation biases the body's fluid immune response toward abnormally immature memory B cells (MB) while damaging plasma cell differentiation.
At the molecular level, TBL1XR1 mutants work together with SMRT/HDAC3 inhibitor complexes to combine MB cell transcription factor (TF) BACH2 at the expense of reproductive center (GC) transcription factor BCL6, leading to pre-memory transcription reprogramming and cell fate bias.
antigen recovery, TBL1XR1 mutant MB cells could not differentiate into plasma cells, but preferred to re-enter the new GC reaction, providing evidence for circulating re-entry into the lymphatic mechanism.
, the TBL1XR1 change led to an amazing esoteric immune cell lymphoma esotesthea, mimicking human disease.
and mouse lymphomas have enlarged MB-like cell populations, which are consistent with the origin of MB cells and reveal unforeseen paths of malignant transformation of the immune system.
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