<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Karmoker JR</submitter><funding>US Government National Institutes of Health</funding><funding>NEI NIH HHS</funding><funding>National Eye Institute</funding><funding>Research to Prevent Blindness</funding><funding>University of Oklahoma Health Sciences Center</funding><pagination>167351</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11330344</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>1870(7)</volume><pubmed_abstract>Injuries to the retinal pigment epithelium (RPE) trigger immune responses, orchestrating interactions within the innate and adaptive immune systems in the outer retina and choroid. We previously reported that interleukin 17 (IL-17) is a pivotal signaling molecule originating from choroidal γδ T cells, exerting protective effects by mediating functional connections between the RPE and subretinal microglia. In this current study, we generated mice with aryl hydrocarbon receptor (AhR) knockout specifically in IL-17-producing cells. These animals had deficiency in IL-17 production from γδ T cells, and exhibited increased sensitivity to both acute and chronic insults targeting the RPE. These findings imply that IL-17 plays a crucial role as a signaling cytokine in preserving the homeostasis of </pubmed_abstract><journal>Biochimica et biophysica acta. Molecular basis of disease</journal><pubmed_title>Aryl hydrocarbon receptor (AhR)-mediated immune responses to degeneration of the retinal pigment epithelium.</pubmed_title><pmcid>PMC11330344</pmcid><funding_grant_id>R01EY034742</funding_grant_id><funding_grant_id>P30 EY021725</funding_grant_id><funding_grant_id>R01 EY034742</funding_grant_id><funding_grant_id>P30EY027125</funding_grant_id><pubmed_authors>Karmoker JR</pubmed_authors><pubmed_authors>Bounds SE</pubmed_authors><pubmed_authors>Cai J</pubmed_authors></additional><is_claimable>false</is_claimable><name>Aryl hydrocarbon receptor (AhR)-mediated immune responses to degeneration of the retinal pigment epithelium.</name><description>Injuries to the retinal pigment epithelium (RPE) trigger immune responses, orchestrating interactions within the innate and adaptive immune systems in the outer retina and choroid. We previously reported that interleukin 17 (IL-17) is a pivotal signaling molecule originating from choroidal γδ T cells, exerting protective effects by mediating functional connections between the RPE and subretinal microglia. In this current study, we generated mice with aryl hydrocarbon receptor (AhR) knockout specifically in IL-17-producing cells. These animals had deficiency in IL-17 production from γδ T cells, and exhibited increased sensitivity to both acute and chronic insults targeting the RPE. These findings imply that IL-17 plays a crucial role as a signaling cytokine in preserving the homeostasis of </description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Oct</publication><modification>2026-06-03T23:58:25.642Z</modification><creation>2026-05-03T03:12:22.733Z</creation></dates><accession>S-EPMC11330344</accession><cross_references><pubmed>39004382</pubmed><doi>10.1016/j.bbadis.2024.167351</doi></cross_references></HashMap>