Authors
Jingjing Wen, Jingcao Huang, Juan Xu, Pan Zhao, Xiaohui Zhao, Siyao He, Linfeng Li, Xiang Liu, Hongmei Luo, Ziyue Mi, Yue Zhang, Qianwen Gao, Haonan Yang, Yu Feng, Xinyu Zhai, Fangfang Wang, Dan Zhang, Li Zhang, Wenjiao Tang, Enguang Bi, Ting Niu, Yuhuan Zheng
Published in
Haematologica. Aug 13, 2026. Epub Aug 13, 2026.
Abstract
Macrophage migration inhibitory factor (MIF), derived from either tumor cells or the tumor microenvironment, promotes multiple myeloma (MM) progression by suppressing T cell-mediated antitumor responses. Here, we demonstrate that MIF drives immune evasion in MM through both TME-mediated and tumor-intrinsic mechanisms. In the TME, MIF promotes the expansion of myeloid-derived suppressor cells (MDSCs) and enhances the expression of immunosuppressive molecules, including CD84, PD-L1, and CD38, thereby augmenting MDSC-mediated immunosuppression and impairing T cell function. In MM cells, MIF suppresses the COPS5/STAT1/NLRC5 signaling axis, resulting in downregulation of the major histocompatibility complex class I (MHC-I) antigen presentation pathway and reduced T cell-mediated cytotoxicity against MM cells. Therapeutically, combined treatment with the MIF inhibitor 4-IPP and dexamethasone delayed MM progression and prolonged survival in a mouse MM model. In summary, our findings reveal MIF as a critical mediator of immune escape in MM and highlight the therapeutic potential of MIF-targeted strategies for MM treatment.
PMID:
42610421
Bibliographic data and abstract were imported from PubMed on 18 Aug 2026.
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