AI Article Synopsis
- * A small percentage of CLL patients (up to 5%) may experience a transformation to a more aggressive form called Richter's syndrome, which negatively impacts prognosis and is linked to decreased levels of NFAT2.
- * The study reveals that targeting the tyrosine kinase LCK, a key regulator of NFAT2 in CLL, can disrupt the anergic state and reactivate BCR signaling, potentially speeding up the progression of CLL.
Article Abstract
Most patients with chronic lymphocytic leukemia (CLL) exhibit an indolent disease course and unresponsive B cell receptors (BCRs) exemplified by an anergic phenotype of their leukemic cells. In up to 5% of patients, CLL transforms from an indolent subtype to an aggressive form of B cell lymphoma (Richter's syndrome), which is associated with worse disease outcome and severe downregulation of NFAT2. Here we show that ablation of the tyrosine kinase LCK, which has previously been characterized as a main NFAT2 target gene in CLL, leads to loss of the anergic phenotype, thereby restoring BCR signaling, which results in an acceleration of CLL. Our study identifies LCK as a main player in mediating BCR unresponsiveness and its role as a crucial regulator of anergy in CLL.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7492521 | PMC |
| http://dx.doi.org/10.3389/fimmu.2020.01995 | DOI Listing |
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