Barinberg D, Sebald H, Gold T, Rai B, Radtke D, Lerm D, Vöhringer D, Jantsch J, Wirtz S, Antonova AU, Colonna M, Bogdan C, Schleicher U (2026)
Publication Type: Journal article
Publication year: 2026
Book Volume: 18
Pages Range: 1292–1317
DOI: 10.1038/s44321-026-00392-x
Eosinophils exhibit antimicrobial, cytotoxic and immunoregulatory effects, but our knowledge of their transcriptional and functional heterogeneity is still limited, especially in non-intestinal tissues. Here, we used a mouse model of chronic cutaneous inflammation elicited by the protozoan pathogen Leishmania mexicana to investigate the function and transcriptional dynamics of skin eosinophils. Infection of C57BL/6 mice triggered local and systemic eosinophilia that was driven by type 2 innate lymphoid cells and interleukin-5. Genetic and pharmacological eosinophil depletion led to an enhanced Th1 response, polarization towards M1-like macrophages and resolution of clinical disease, despite an unexpected simultaneous upregulation of IL-4. Single-cell transcriptomics revealed a skin-imprinted trajectory of inflammatory eosinophils that strongly expressed the glucose transporter Slc2a3 (GLUT3) These eosinophils impeded the function of Th1 cells by forming a competitive metabolic niche through preferential glucose uptake. Our findings uncover an inflammatory, metabolically reprogrammed eosinophil population that promotes chronic skin inflammation by limiting protective T cell responses.
APA:
Barinberg, D., Sebald, H., Gold, T., Rai, B., Radtke, D., Lerm, D.,... Schleicher, U. (2026). Metabolically reprogrammed eosinophils impair T cell immunity and cause chronic skin infection. Embo Molecular Medicine, 18, 1292–1317. https://doi.org/10.1038/s44321-026-00392-x
MLA:
Barinberg, David, et al. "Metabolically reprogrammed eosinophils impair T cell immunity and cause chronic skin infection." Embo Molecular Medicine 18 (2026): 1292–1317.
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