AI Article Synopsis
- Janus kinase (JAK) inhibitors are commonly used for treating autoimmune and inflammatory diseases, impacting natural killer (NK) cells and innate lymphoid cells (ILCs).
- Research indicates that in mice, liver ILC1s are less affected by JAK inhibitors compared to NK cells in various organs.
- The study found that JAK inhibition altered genes related to cell cycle and apoptosis in both cell types, but ILC1s were protected by high levels of the antiapoptotic gene Bcl2, suggesting a need for further understanding of these mechanisms for clinical applications.
Article Abstract
Janus kinase (JAK) inhibitors are widely used in the treatment of multiple autoimmune and inflammatory diseases. Immunologic and transcriptomic profiling have revealed major alterations on natural killer (NK) cell homeostasis associated with JAK inhibitions, while information on other innate lymphoid cells (ILCs) is still lacking. Herein, we observed that, in mice, the homeostatic pool of liver ILC1 was less affected by JAK inhibitors compared to the pool of NK cells present in the liver, spleen and bone marrow. JAK inhibition had overlapping effects on the transcriptome of both subsets, mainly affecting genes regulating cell cycle and apoptosis. However, the differential impact of JAK inhibition was linked to the high levels of the antiapoptotic gene Bcl2 expressed by ILC1. Our findings provide mechanistic explanations for the effects of JAK inhibitors on NK cells and ILC1 which could be of major clinically relevance.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6930870 | PMC |
| http://dx.doi.org/10.3389/fimmu.2019.02972 | DOI Listing |
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