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Brain-wide mapping of immune receptors uncovers a neuro-modulatory role of interleukin-17E and the receptor IL-17RB.

ABSTRACT: Cytokines engage with their receptor complexes to orchestrate diverse processes -- from immune responses to modulating behaviors. Interleukin-17A (IL-17A) mediates protective immune responses by binding to IL-17 receptor A (IL-17A) and IL-17RC subunits. IL-17A also modulates social interaction, but the role of cytokine receptors in this process and their expression in the brain is not well characterized. Here, we mapped the brain-region-specific expression of all major IL-17R subunits and discovered that IL-17RB, not IL-17RC, expression in the cortex plays a role in social behaviors. Through genetic experiments, we further showed that IL-17E, a ligand for the IL-17RB-containing receptor complex, enhances social interaction by directly impacting IL-17RB-expressing neurons in the cortex. These findings highlight a novel IL-17 circuit operating within the cortex to modulate social behaviors. Thus, characterizing spatially restricted cytokine receptor expression can be leveraged to elucidate how cytokines function as critical messengers mediating neuro-immune interactions to shape animal behaviors.

ORGANISM(S): Mus musculus

PROVIDER: GSE286801 | GEO | 2025/04/07

REPOSITORIES: GEO

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Project description:Background: Chronic rhinosinusitis with nasal polyposis (CRSwNP) in western countries is characterized by eosinophilia, IgE production and Th2 cytokine expression. Type 2 innate lymphoid cells (ILC2) from polyps produce IL-5 and IL-13 in response to IL-25 and IL-33 although the relevance of this axis to local mucosal T cell responses is unknown. Objective: To investigate the role of the IL-25/IL-33 axis in local mucosal T cell responses in CRSwNP. Methods: Polyp tissue and blood were obtained from patients undergoing nasal polypectomy. Control nasal biopsies and blood were obtained from healthy volunteers. Tissue was cultured in a short-term explant model. T cell surface phenotype/intracellular cytokines were assessed by flow cytometry. TCR VÎ² analysis was performed with the immunoSEQ assay. Microarrays were performed for gene expression analysis. Results: Using nasal polyp tissue, numerous IL-25 receptor (IL-17RB) positive polarized Th2 cells were identified which were absent in the healthy nasal mucosa and periphery. IL-17RB+CD4+ polyp Th2 cells co-expressed ST2 (IL-33 receptor) and responded to IL-25 and IL-33 with enhanced IL-5 and IL-13 production. Within IL-17RB+CD4+ T cells several identical TCR VÎ² CDR3 sequences were identified in different subjects suggesting clonal expansion driven by a common antigen. Abundant IL-17 producing T cells were observed in healthy nasal mucosal and polyp populations with Th17-related genes the most overexpressed compared to peripheral blood T cells. Conclusion: IL-25 and IL-33 may interact locally with IL-17RB+ST2+ polyp T cells to augment Th2 responses in CRSwNP. A local Th17 response may be the default signature in healthy nasal mucosal immune homeostasis. Three biological replicates. T-helper cells were isolated nasal polyps by explant culture from patients with chronic rhinosinusitis. Cells were then sorted based upon expression of IL17RB by flow cytometric sorting. Resting and activated IL-17RB+ve cells were compared with resting and activated IL-17RB-ve cells.

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Brain-wide mapping of immune receptors uncovers a neuro-modulatory role of interleukin-17E and the receptor IL-17RB.

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