Journal
CELLULAR & MOLECULAR IMMUNOLOGY
Volume 20, Issue 11, Pages 1367-1378Publisher
CHIN SOCIETY IMMUNOLOGY
DOI: 10.1038/s41423-023-01081-2
Keywords
FBXO38; Macrophage polarization; Tumor progression; Colitis
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Macrophages are versatile cells that can be activated by different stimuli to differentiate into distinct subsets. FBXO38, a protein identified in this study, was found to promote immunosuppressive function in macrophages without affecting other macrophage functions. Further investigation revealed that deletion of FBXO38 in macrophages can block tumor development and protect against colitis.
Macrophages are highly plastic cells that differentially regulate multiple pathological conditions, including cancer and autoimmune diseases. In response to various stimuli, macrophages activate different intrinsic signaling pathways and polarize into distinct macrophage subsets. We aimed to identify key new effectors that could control macrophage polarization and impact the development of cancer or colitis. Following treatment with the supernatants of tumor cells, macrophages showed an upregulation in Fbxo38 expression. Subsequently, we further identified that FBXO38 promotes macrophage immunosuppressive function by upregulating the expression of M2-like genes via MAPK and IRF4 signaling without affecting M1-like macrophage polarization. Deletion of Fbxo38 in macrophages was found to block tumor development and protect against DSS-induced colitis. Considering the distinct regulation of tumor development by FBXO38 in T cells and macrophages, we suggest that a comprehensive understanding of FBXO38 function in different cell types is critical for its further translational usage.
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