{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Dinarello A"],"funding":["NIAID NIH HHS","NIH","NIGMS NIH HHS","NIH HHS"],"pagination":["e2306476120"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10636342"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["120(45)"],"pubmed_abstract":["The IL-1 Family member IL-38 has been characterized primarily as an antiinflammatory cytokine in human and mouse models of systemic diseases. Here, we examined the role of IL-38 in the murine small intestine (SI). Immunostaining of SI revealed that IL-38 expression partially confines to intestinal stem cells. Cultures of intestinal organoids reveal IL-38 functions as a growth factor by increasing organoid size via inducing WNT3a. In contrast, organoids from IL-38-deficient mice develop more slowly. This reduction in size is likely due to the downregulation of intestinal stemness markers (i.e., <i>Fzd5</i>, <i>Ephb2</i>, and <i>Olfm4</i>) expression compared with wild-type organoids. The IL-38 binding to IL-1R6 and IL-1R9 is still a matter of debate. Therefore, to analyze the molecular mech"],"journal":["Proceedings of the National Academy of Sciences of the United States of America"],"pubmed_title":["IL-38 regulates intestinal stem cell homeostasis by inducing WNT signaling and beneficial IL-1β secretion."],"pmcid":["PMC10636342"],"funding_grant_id":["R01 GM139892","R03 AI151651","AI 15614","R01 AI015614","R56 AI015614","R03 AI156560"],"pubmed_authors":["Amo-Aparicio J","Tesoriere A","de Graaf DM","Marchetti C","Ghirardo R","Redzic JS","Li S","Azam T","Atif SM","Dinarello A","May M","Webber WS","Eisenmesser EZ","Gaballa JM","Dinarello CA"],"additional_accession":[]},"is_claimable":false,"name":"IL-38 regulates intestinal stem cell homeostasis by inducing WNT signaling and beneficial IL-1β secretion.","description":"The IL-1 Family member IL-38 has been characterized primarily as an antiinflammatory cytokine in human and mouse models of systemic diseases. Here, we examined the role of IL-38 in the murine small intestine (SI). Immunostaining of SI revealed that IL-38 expression partially confines to intestinal stem cells. Cultures of intestinal organoids reveal IL-38 functions as a growth factor by increasing organoid size via inducing WNT3a. In contrast, organoids from IL-38-deficient mice develop more slowly. This reduction in size is likely due to the downregulation of intestinal stemness markers (i.e., <i>Fzd5</i>, <i>Ephb2</i>, and <i>Olfm4</i>) expression compared with wild-type organoids. The IL-38 binding to IL-1R6 and IL-1R9 is still a matter of debate. Therefore, to analyze the molecular mech","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Nov","modification":"2026-06-01T10:51:05.136Z","creation":"2026-04-08T11:32:18.377Z"},"accession":"S-EPMC10636342","cross_references":{"pubmed":["37906644"],"doi":["10.1073/pnas.2306476120"]}}