2026/03/11 by David Barinberg, Heidi Sebald, Tobias Gold +10 · 1 voice · 1 citation
Immunology and Microbiology · Medicine · #IL-33, ST2, and ILC Pathways #Eosinophilic Disorders and Syndromes #Immune cells in cancer
paper · pdf · doi:10.1038/s44321-026-00392-x
openalex publication_date 2026/03/11 · openalex created_date 2026/03/13 · openalex updated_date 2026/07/29
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.