ArticleFrontiers in immunology2023
Soluble CD83 modulates human-monocyte-derived macrophages toward alternative phenotype, function, and metabolism.
Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 3 citations in OpenAlex.
- Langerhans Cell Modulation in Atopic Dermatitis Is TLR2/SOCS1-Dependent and JAK Inhibitor-Sensitive.Allergy · 2025Article
- Reduced tolerogenic factor sCD83 in NMOSD and relapsing MOGAD: a potential new therapeutic pathway.Frontiers in immunology · 2025Article
- Soluble CD83 Accelerates Wound Healing and Attenuates Inflammatory Responses Induced by Chronic Wound Fluid in a Human 3D in Vitro Wound Healing Model.Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair SocietyArticle
Corrections and comments
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Authors and funding
15 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alterations in macrophage (Mφ) polarization, function, and metabolic signature can foster development of chronic diseases, such as autoimmunity or fibrotic tissue remodeling. Thus, identification of novel therapeutic agents that modulate human Mφ biology is crucial for treatment of such conditions. Herein, we demonstrate that the soluble CD83 (sCD83) protein induces pro-resolving features in human monocyte-derived Mφ biology. We show that sCD83 strikingly increases the expression of inhibitory molecules including ILT-2 (immunoglobulin-like transcript 2), ILT-4, ILT-5, and CD163, whereas activation markers, such as MHC-II and MSR-1, were significantly downregulated. This goes along with a decreased capacity to stimulate alloreactive T cells in mixed lymphocyte reaction (MLR) assays. Bulk RNA sequencing and pathway analyses revealed that sCD83 downregulates pathways associated with pro-inflammatory, classically activated Mφ (CAM) differentiation including HIF-1A, IL-6, and cytokine storm, whereas pathways related to alternative Mφ activation and liver X receptor were significantly induced. By using the LXR pathway antagonist GSK2033, we show that transcription of specific genes (e.g.,
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Registered trials
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