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Please use this identifier to cite or link to this item: https://hdl.handle.net/2445/146501
SLAMF5 enhances autophagy and fine-tunes cytokine response in monocyte-derived dendritic cells via stabilization of Interferon regulatory Factor 8
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Signaling lymphocyte activation molecule family (SLAMF) receptors are essential regulators of innate and adaptive immune responses. The function of SLAMF5/CD84, a family member with almost ubiquitous expression within the hematopoietic lineage is poorly defined. In this article, we provide evidence that in human monocyte-derived dendritic cells (moDCs) SLAMF5 increases autophagy, a degradative pathway, which is highly active in dendritic cells (DCs) and plays a critical role in orchestration of the immune response. While investigating the underlying mechanism, we found that SLAMF5 inhibited proteolytic degradation of interferon regulatory factor 8 (IRF8) a master regulator of the autophagy process by a mechanism dependent on the E3-ubiquitin ligase tripartite motif-containing protein 21 (TRIM21). Furthermore, we demonstrate that SLAMF5 influences the ratio of CD1a+ cells in differentiating DCs and partakes in the regulation of IL-1β, IL-23, and IL-12 production in LPS/IFNγ-activated moDCs in a manner that is consistent with its effect on IRF8 stability. In summary, our experiments identified SLAMF5 as a novel cell surface receptor modulator of autophagy and revealed an unexpected link between the SLAMF and IRF8 signaling pathways, both implicated in multiple human pathologies.
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AGOD, Zsofia, et al. SLAMF5 enhances autophagy and fine-tunes cytokine response in monocyte-derived dendritic cells via stabilization of Interferon regulatory Factor 8. Frontiers in Immunology. 2018. Vol. 9, num. 62. ISSN 1664-3224. [consulted: 11 of October of 2026]. Available at: https://hdl.handle.net/2445/146501