IL-22RA1 is highly expressed on pancreatic islets and absent on immune cells. Here, the authors investigate its role by generating animals that lack IL-22RA1 on beta cells and reveal IL22RA1 signalling is critical for insulin biosynthesis and beta-cell health, evidenced by its regulation of MHC II expression and its suppressive effect on inflammation and cellular stress.
Sajiir, H., Wong, K. Y., Muller, A., Keshvari, S., Burr, L., Aiello, E., Mezza, T., Giaccari, A., Sebastiani, G., Dotta, F., Ramm, G. A., Macdonald, G. A., Mcguckin, M. A., Prins, J. B., Hasnain, S. Z., Pancreatic beta-cell IL-22 receptor deficiency induces age-dependent dysregulation of insulin biosynthesis and systemic glucose homeostasis, <<NATURE COMMUNICATIONS>>, 2024; 15 (1): N/A-N/A. [doi:10.1038/s41467-024-48320-2] [https://hdl.handle.net/10807/302095]
Pancreatic beta-cell IL-22 receptor deficiency induces age-dependent dysregulation of insulin biosynthesis and systemic glucose homeostasis
Mezza, Teresa;Giaccari, Andrea;
2024
Abstract
IL-22RA1 is highly expressed on pancreatic islets and absent on immune cells. Here, the authors investigate its role by generating animals that lack IL-22RA1 on beta cells and reveal IL22RA1 signalling is critical for insulin biosynthesis and beta-cell health, evidenced by its regulation of MHC II expression and its suppressive effect on inflammation and cellular stress.
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