AI Article Synopsis

  • Kinase inhibitors, like dasatinib, are promising for targeted cancer therapy but also have effects on the immune system, particularly T-cells and NK-cells.
  • Research suggests dasatinib may also affect non-conventional T-αβ cell subsets, such as iNKT and a new CD8 T-cell subset, by promoting an activated and anti-tumor phenotype.
  • In both mice and humans, dasatinib treatment increased the frequency of these innate T-cell subsets, showing its potential to enhance immune responses and paving the way for combined chemotherapy and immunotherapy approaches.

Article Abstract

Kinase inhibitors hold great potential as targeted therapy against malignant cells. Among them, the tyrosine kinase inhibitor dasatinib is known for a number of clinically relevant off-target actions, attributed in part to effects on components of the immune system, especially conventional T-cells and natural killer (NK)-cells. Here, we have hypothesized that dasatinib also influences non-conventional T-αβ cell subsets known for their potential anti-tumoral properties, namely iNKT cells and the distinct new innate CD8 T-cell subset. In mice, where the two subsets were originally characterized, an activated state of iNKT cells associated with a shift toward an iNKT cell Th1-phenotype was observed after dasatinib treatment in vivo. Despite decreased frequency of the total memory CD8 T-cell compartment, the proportion of innate-memory CD8 T-cells and their IFNγ expression in response to an innate-like stimulation increased in response to dasatinib. Lastly, in patients administered with dasatinib for the treatment of BCR-ABL-positive leukemias, we provided the proof of concept that the kinase inhibitor also influences the two innate T-cell subsets in humans, as attested by their increased frequency in the peripheral blood. These data highlight the potential immunostimulatory capacity of dasatinib on innate T-αβ cells, thereby opening new opportunities for chemoimmunotherapy.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7039999PMC
http://dx.doi.org/10.1038/s41598-020-60195-zDOI Listing

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