Ask about this productRelated genes to: RORC 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: RORC antibody
Related articles to: RORC antibody
- 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 - Beyond their well-established roles in type 3 immunity, RORγt innate immune cells are also essential for secondary lymphoid organ (SLO) formation and gut homeostasis. However, the transcriptional mechanisms governing RORγt expression in these cells, including group 3 innate lymphoid cells (ILC3s), lymphoid tissue inducer (LTi) cells, and antigen-presenting cells (APCs), remain largely unresolved. Here, we identified two key cis-regulatory elements within conserved non-coding sequences (CNS)9 and 11 in the Rorc locus, which were sequentially utilized during differentiation. Initially, Runx-binding sites in CNS11 established chromatin accessibility as early as the hematopoietic stem cell (HSC) stage. Disruption of this chromatin priming prevented subsequent transcriptional activation, thereby abolishing the initial induction of RORγt in these cells. At later stages, CNS9 played a critical role, particularly in the development of RORγt⁺ APCs, contributing to colonic peripheral Treg (pTreg) cell induction. This hierarchical transcriptional regulation was essential for SLO formation and postnatal type 3 immunity and for restraining excessive intestinal type 2 immune responses through pTreg cell induction. - Source: PubMed
Publication date: 2026/03/24
Fukui TakumaWatanabe MiyukiKobayashi ReoYamada TaishoNakano KentaTanaka KaoriHarada AkihitoOkamura TadashiSonoda Koh-HeiOhkawa YasuyukiSumiya ErikoShao RuiqiSuyama MikitaTaniuchi IchiroKojo SatoshiSawa Shinichiro