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• W3213161841 endingPage "101517" @default.
• W3213161841 startingPage "101517" @default.
• W3213161841 abstract "IL-34 is a cytokine that shares one of its receptors with CSF-1. It has long been thought that CSF-1 receptor (CSF-1R) receives signals only from CSF-1, but the identification of IL-34 reversed this stereotype. Regardless of low structural homology, IL-34 and CSF-1 emanate similar downstream signaling through binding to CSF-1R and provoke similar but different physiological events afterward. In addition to CSF-1R, protein-tyrosine phosphatase (PTP)-ζ and Syndecan-1 were also identified as IL-34 receptors and shown to be at play. Although IL-34 expression is limited to particular tissues in physiological conditions, previous studies have revealed that it is upregulated in several diseases. In cancer, IL-34 is produced by several types of tumor cells and contributes to therapy resistance and disease progression. A recent study has demonstrated that tumor cell-derived IL-34 abrogates immunotherapy efficacy through myeloid cell remodeling. On the other hand, IL-34 expression is downregulated in some brain and dermal disorders. Despite accumulating insights, our understanding of IL-34 may not be even close to its nature. This review aims to comprehensively describe the physiological and pathological roles of IL-34 based on its similarity and differences to CSF-1 and discuss the rationale for its disease-dependent expression pattern." @default.
• W3213161841 created "2021-11-22" @default.
• W3213161841 creator A5025136502 @default.
• W3213161841 creator A5078219269 @default.
• W3213161841 creator A5089794335 @default.
• W3213161841 date "2021-04-01" @default.
• W3213161841 modified "2023-10-18" @default.
• W3213161841 title "IL-34, the rationale for its expression in physiological and pathological conditions" @default.
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• W3213161841 doi "https://doi.org/10.1016/j.smim.2021.101517" @default.
• W3213161841 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/34774392" @default.
• W3213161841 hasPublicationYear "2021" @default.
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