Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy · 2026
IFNα2b modulates anti-tumor immune responses involving STAT3-associated dendritic cell dysfunction in JAK2v617f-positive myeloproliferative neoplasms.
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Fang Lijun, Fu Rongfeng, Dong Huan, Zhang Wenhui, Gao Yuchen, Xu Yanmei, Gu Wenjing, Liu Zixuan, Li Huiyuan, Wang Wentian, Pei Xiaolei, Chi Ying, Zhou Yuan, Wei Jun, Wang Ying, Zhang Lei
Аннотация
AIMS: To define JAK2v617f-induced immune alterations, focusing on STAT3-mediated dendritic cell dysfunction, and evaluate whether IFNα2b restores anti-tumor immunity in JAK2v617f-positive myeloproliferative neoplasms.
METHODS: Integrated flow cytometry and single-cell RNA sequencing profiled immune landscapes and signaling pathways, while functional assays assessed dendritic cell differentiation, T cell activation, and IFNα2b-mediated immune restoration.
RESULTS: JAK2v617f was associated with increased STAT3 activation in myeloid cells, accompanied by elevated expression of immunosuppressive mediators such as FGL2, impaired monocyte-to-DC differentiation, reduced cDC1/cDC2 subsets, and diminished T cell activation, consistent with an immunosuppressive immune landscape. IFNα2b treatment was associated with attenuation of STAT3/FGL2 signaling and partial restoration of DC-mediated T cell priming, with more pronounced immunomodulatory effects observed in JAK2v617f-positive myeloproliferative neoplasms compared with other subtypes.
CONCLUSIONS: Our findings indicate that JAK2v617f is associated with STAT3-dependent dendritic cell dysfunction that contributes to an immunosuppressive milieu. IFNα2b modulates this pathway and partially restores DC-T cell interactions, highlighting its potential as an immunomodulatory strategy in JAK2v617f-positive myeloproliferative neoplasms.
METHODS: Integrated flow cytometry and single-cell RNA sequencing profiled immune landscapes and signaling pathways, while functional assays assessed dendritic cell differentiation, T cell activation, and IFNα2b-mediated immune restoration.
RESULTS: JAK2v617f was associated with increased STAT3 activation in myeloid cells, accompanied by elevated expression of immunosuppressive mediators such as FGL2, impaired monocyte-to-DC differentiation, reduced cDC1/cDC2 subsets, and diminished T cell activation, consistent with an immunosuppressive immune landscape. IFNα2b treatment was associated with attenuation of STAT3/FGL2 signaling and partial restoration of DC-mediated T cell priming, with more pronounced immunomodulatory effects observed in JAK2v617f-positive myeloproliferative neoplasms compared with other subtypes.
CONCLUSIONS: Our findings indicate that JAK2v617f is associated with STAT3-dependent dendritic cell dysfunction that contributes to an immunosuppressive milieu. IFNα2b modulates this pathway and partially restores DC-T cell interactions, highlighting its potential as an immunomodulatory strategy in JAK2v617f-positive myeloproliferative neoplasms.