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- Asada, N, et al.
(author)
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Tissue-resident memory T cells in the kidney
- 2022
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In: Seminars in immunopathology. - : Springer Science and Business Media LLC. - 1863-2300 .- 1863-2297. ; 44:6, s. 801-811
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Journal article (peer-reviewed)abstract
- The identification of tissue-resident memory T cells (TRMcells) has significantly improved our understanding of immunity. In the last decade, studies have demonstrated that TRMcells are induced after an acute T-cell response, remain in peripheral organs for several years, and contribute to both an efficient host defense and autoimmune disease. TRMcells are found in the kidneys of healthy individuals and patients with various kidney diseases. A better understanding of these cells and their therapeutic targeting might provide new treatment options for infections, autoimmune diseases, graft rejection, and cancer. In this review, we address the definition, phenotype, and developmental mechanisms of TRMcells. Then, we further discuss the current understanding of TRMcells in kidney diseases, such as infection, autoimmune disease, cancer, and graft rejection after transplantation.
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- Jimenez, MT, et al.
(author)
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The miR-181 family regulates colonic inflammation through its activity in the intestinal epithelium
- 2022
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In: The Journal of experimental medicine. - : Rockefeller University Press. - 1540-9538 .- 0022-1007. ; 219:12
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Journal article (peer-reviewed)abstract
- The intestinal epithelium is a key physical interface that integrates dietary and microbial signals to regulate nutrient uptake and mucosal immune cell function. The transcriptional programs that regulate intestinal epithelial cell (IEC) quiescence, proliferation, and differentiation have been well characterized. However, how gene expression networks critical for IECs are posttranscriptionally regulated during homeostasis or inflammatory disease remains poorly understood. Herein, we show that a conserved family of microRNAs, miR-181, is significantly downregulated in IECs from patients with inflammatory bowel disease and mice with chemical-induced colitis. Strikingly, we showed that miR-181 expression within IECs, but not the hematopoietic system, is required for protection against severe colonic inflammation in response to epithelial injury in mice. Mechanistically, we showed that miR-181 expression increases the proliferative capacity of IECs, likely through the regulation of Wnt signaling, independently of the gut microbiota composition. As epithelial reconstitution is crucial to restore intestinal homeostasis after injury, the miR-181 family represents a potential therapeutic target against severe intestinal inflammation.
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