Ask about this productRelated genes to: NR1F3 antibody
- Gene:
- RORC NIH gene
- Name:
- RAR related orphan receptor C
- Previous symbol:
- -
- Synonyms:
- RZRG, RORG, NR1F3, TOR
- Chromosome:
- 1q21
- Locus Type:
- gene with protein product
- Date approved:
- 1995-04-13
- Date modifiied:
- 2019-04-23
Related products to: NR1F3 antibody
Related articles to: NR1F3 antibody
- Type 2 high asthma is driven by coordinated GATA3 dependent programs in CD4 T cells and group 2 innate lymphoid cells (ILC2). Although biologics targeting IL4, IL5, or IL13 benefit subsets of patients, many remain symptomatic, suggesting that upstream regulatory mechanisms may sustain type 2 inflammation. We investigated whether HuR (ELAVL1), an RNA-binding protein that stabilizes GATA3 and Th2 cytokines mRNA, regulates type 2 inflammatory programs in allergic asthma. Using a house dust mite (HDM) model in vivo, HuR inhibition with the small molecule KH3 reduced lung inflammation, suppressed Th2 cytokine expression, accelerated Gata3 mRNA decay in lung CD4 T cells, and attenuated airway hyperresponsiveness toward control levels. In ex vivo activated human lung CD4 T cells, KH3 accelerated GATA3 mRNA decay with minimal effects on RORC or TBX21 and selectively reduced Th2 cytokine secretion, while IL10 and IL2 were unchanged. Similarly, ILC2s isolated from peripheral blood mononuclear cells (PBMCs) of type 2 high asthmatic donors showed reduced GATA3 mRNA stability and diminished Th2 cytokine production following KH3 treatment. Single-cell transcriptomic analysis of bronchoalveolar lavage fluid after allergen challenge demonstrated co-enrichment of ELAVL1 and GATA3 within Th2 clusters in human airways. Together, these findings identify HuR as a post-transcriptional regulator of GATA3 driven type 2 inflammation in allergic asthma. - Source: PubMed
Publication date: 2026/04/27
Atasoy UlusFattahi FatemehYaekle LauraHolden JuliaTepper BrandonHussein KareemMeier JoshuaXu LiangNerella SrilaxmiLei JingBentley KelleyHershenson MarcHuang Steven K - Myocarditis is an inflammatory cardiac disease in which Th17-driven immune responses contribute to progression toward dilated cardiomyopathy and heart failure. Current therapies mainly rely on corticosteroids but lack specificity, while the role of miR-721, synthesized by Th17 cells, remains largely unexplored in disease pathogenesis. - Source: PubMed
Publication date: 2026/03/26
Ruiz-Fernández IgnacioSánchez-Díaz RaquelBlanco-Domínguez RafaelOrtega-Sollero EnriqueOrtego-Moltó RuthQuiroga-Ortiz Danielade la Fuente HortensiaMartínez-González JoséJiménez-Borreguero Luis JesúsLópez-Melgar BeatrizRivero FernandoAlfonso FernandoSánchez-Madrid FranciscoRicote MercedesMartín Pilar - LINGO4 is a leucine-rich repeat and immunoglobulin-like domain-containing transmembrane protein encoded immediately adjacent to Rorc, the gene for RORγt, raising the possibility that it contributes to the biology of RORγt+ lymphocytes. However, its impact on these cells and resistance to enteric infections has remained unknown. Here, we identify LINGO4 as a critical regulator of group 3 innate lymphoid cells (ILC3s). Lingo4-/- ILC3s exhibit a profound, cell-intrinsic defect in IL-22 production linked to impaired STAT3 activation, mitochondrial dysfunction, elevated ROS, and increased apoptosis. In vivo, Lingo4 deficiency also drives a dysbiotic gut microbiota, resulting in an additional, microbiota-dependent loss of ILC3s. These combined defects increase susceptibility to Clostridioides difficile and Citrobacter rodentium, whereas IL-22 reduction in Lingo4-/- mice confers protection against Salmonellatyphimurium. Immunoprecipitation of tagged LINGO4 reveals interaction networks enriched in mitochondrial pathways, providing mechanistic insight into its role in ILC3 metabolic fitness and intestinal immunity. - Source: PubMed
Publication date: 2026/04/28
Fachi José LTrsan TihanaSécca Cristianede Oliveira SarahRodovalho Vinícius RRodrigues Patrick FernandesBeatty Wandy LSudan RakiWu ShitongBhattarai BishanPanda Santosh KCella MarinaGilfillan SusanColonna Marco - γδ T cells boost inflammatory responses and exacerbate tissue damage after ischemic stroke. However, the origin, dynamics, and tissue adaptation of γδ T cells in the ischemic brain and its border regions remain poorly understood. A systematic integration of large-scale datasets is urgently needed. Here, we investigated the impact of ischemic stroke on the state of meningeal and brain-infiltrating γδ T cells and explored their potential contributions to post-stroke inflammation. - Source: PubMed
Publication date: 2026/04/09
Zha MingmingJander AlinaCai HaodiPiepke MariusDegenhardt KarolineWinter LeoMagnus TimGelderblom Mathias - Memory T helper (Th) cells sustain protective recall responses but can also drive chronic inflammation, necessitating precise regulation of their effector programs. Although Th cells produce acetylcholine (ACh) and express nicotinic acetylcholine receptors (nAChRs), the contribution of nAChRs to human memory Th function across central (Tcm) and effector (Tem) subsets is poorly defined. We examined the effect of nicotine and GTS-21, a compound previously described as targeting α7nAChR, on total memory Th cells and purified Tcm and Tem from healthy participants. Nicotine or GTS-21 diminished IFN-γ, IL-4, and IL-17A secretion, downregulated TBX21, GATA3, and RORC, and reduced NF-κB p65 phosphorylation in total memory Th cells. Disruption of CHRNA7 abolished nicotine-mediated suppression but did not eliminate the inhibitory effects of GTS-21. Within CCR7-defined subsets, nicotine and GTS-21 lowered Th1/Th2/Th17 frequencies in Tcm, but not in Tem. In purified subsets, nicotine suppressed IFN-γ, IL-4, IL-17A, IL-21, BCL6, and CD40L selectively in Tcm, whereas GTS-21 suppressed them in both Tcm and Tem. Collectively, nicotine engages an α7nAChR-dependent checkpoint that preferentially regulates Tcm responses, while GTS-21 exerts broader suppressive effects not fully explained by α7nAChR loss. This cholinergic checkpoint in Tcm may limit Tfh-associated help and pathogenic recall responses in immune-mediated disease. - Source: PubMed
Gholizadeh FatemehHajiaghayi MehriRahbari NiloufarChoi Jennifer SHeidt SamanthaComo AlexiaKazerouni MaryamKargar MelikaPinard-LaRoche AudeShih Steve C CDarlington Peter J