Blood: JAK/STAT signal suppression enhances the sensitivity of CD8 T cells to dexamethasone-induced apoptosis
Last Update: 2020-06-16
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Cytokine storm syndrome (CSS) is a severe hyper-inflammatory state characterized by overactivation of the immune system, which can lead to organ damage and patient deathPhytopha lymphatic tissue cytomohyperriatic (HLH) is a typical CSS with a five-year survival rate of only 60%, a disease often associated with cytotoxic genetic defects mediated by cellsHLH's first-line treatments include glucocorticoid disemine (DEX) and chemotherapy drug etoposideHowever, many patients are not tolerant of this treatment or relapse after initial treatment is remissionIt is worth noting that in HLH, multiple cytokines were elevated, activating the JAK/STAT pathway, and the JAK1/2 inhibitor Russotinib (RUX) had shown efficacy in the HLH model in mice and in human patients with refracted diseasesRecently, researchers found that cytokine-induced JAK/STAT signals mediated resistance of T-cell acute lymphoblastic leukemia (T-ALL) cells to dexamethasone, which RUX can effectively reverseBased on these findings, Meyer et alhypothesized that cytokine-mediated JAK/STAT signals may also promote HLH's dexamethasone resistance, which RUX therapy may or may overcomeThrough in vitro experiments, Meyer et aldemonstrated that HLH's hypercell kinase mia reduced the apoptosis potential of CD8 T cells and led to the relative resistance of dexamethasone in HLH mouse models and primary patient samplesAfter exposure to RUX, this apoptosis potential is restored, thereby enhancing the sensitivity of CD8 T cells to dexamethasone-induced apoptosm in vitro and significantly reducing the manifestations of invivia osmology pathology and HLH diseaseIn summary, the results of this study provide a theoretical basis for the combined use of DEX and RUX to enhance the lymphtoxicity effect of DEX to improve the prognosis of HLH and related CSS patients
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