Metabolically reprogrammed eosinophils impair T cell immunity and cause chronic skin infection

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

Journal

Book Volume: 18

Pages Range: 1292–1317

DOI: 10.1038/s44321-026-00392-x

Abstract

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.

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How to cite

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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