Ask about this productRelated genes to: IL15 protein
- Gene:
- IL2RB NIH gene
- Name:
- interleukin 2 receptor subunit beta
- Previous symbol:
- IL15RB
- Synonyms:
- CD122
- Chromosome:
- 22q12.3
- Locus Type:
- gene with protein product
- Date approved:
- 1990-01-22
- Date modifiied:
- 2016-10-11
- Gene:
- IL15 NIH gene
- Name:
- interleukin 15
- Previous symbol:
- -
- Synonyms:
- IL-15, MGC9721
- Chromosome:
- 4q31.21
- Locus Type:
- gene with protein product
- Date approved:
- 1994-07-11
- Date modifiied:
- 2016-10-05
Related products to: IL15 protein
Related articles to: IL15 protein
- Ulcerative colitis (UC) is a chronic gastrointestinal condition with high morbidity. Modern therapies have revolutionized the care of UC, but 10% to 25% of patients do not respond to treatments and many progress to surgery. Thus, developing new treatments remains an important goal in UC. T cells, especially T helper 17 (Th17) cells, are linked with the pathogenesis of UC and are thought to be major targets of medications in UC. Therefore, we considered cytokines that may regulate pathogenic T cells in UC, focusing on cytokines that regulate T cells in tissue, as the intestinal microenvironment contains specialized noncirculating T cell subsets. Using public sequencing datasets, we identified that the IL15 axis is upregulated in UC and CD4+ T cells that express the specificity conferring receptor for IL-15 (IL-2RB) exhibit a pathogenic Th17 signature. Using a combination of murine models and human biospecimens, we verified that pathogenic Th17 cells express IL-2RB. IL-15 was redundant for Th17 differentiation, but IL-15 could activate terminally differentiated Th17 cells in the colon in a JAK1-dependent manner. Thus, we found that the IL15 axis is upregulated in UC and that IL-15 can activate inflammatory Th17 cells in the colon, raising the possibility that IL-15 is a potential target for UC treatments. - Source: PubMed
Hou GuoqingLee AllenGolob Jonathan LGrasberger HelmutBerinstein ElliottSwanson Benjamin JBishu Shreenath RZataari Mohamed ElKhaykin ValerieBerinstein Jeff AFry ChristopherNemzek JeanKamada NobuhikoKao JohnBishu Shrinivas - Vitiligo is a chronic autoimmune disorder in which melanocyte-specific CD8 T cells destroy pigment-forming cells, producing persistent depigmented macules. Recurrence after treatment implicates tissue-resident memory T (TRM) cells that are maintained by interleukin-15 (IL-15) signaling. Here we review current insights into TRM-cell biology, summarize experimental and emerging clinical data targeting the IL-15/CD122 axis-including the ongoing Phase 2a AMG 714 trial-and discuss combination strategies with approved topical Janus kinase inhibitors such as ruxolitinib cream. Disrupting IL-15 may offer durable repigmentation with minimal systemic immunosuppression. - Source: PubMed
Publication date: 2025/07/28
Su XiangxiLiu Fang - Natural killer (NK) cell homeostasis and effector functions require context-dependent signaling via numerous receptors, including the interleukin-15 receptor (IL-15R). Post-translational modifications can regulate receptor signaling, impacting receptor turnover and trafficking. Core fucosylation is one such modification known to impact receptor expression and is uniquely mediated by fucosyltransferase 8 (FUT8). We identified FUT8 as an essential gene required for IL-15R responsiveness in a human NK cell genome-wide CRISPR screen. To further validate core fucosylation in IL-15R signaling and NK cell biology, mice lacking Fut8 in NK cells (Fut8Ncr1) were generated. The loss of core fucose in murine NK cells resulted in severe NK cell lymphopenia, with a reduction in IL-15Rβ (IL-2RB/CD122) expression, impairing in vivo homeostatic proliferation. The loss of FUT8 also decreased NK cell cytotoxicity, tumor immunity, and early viral immunity. Taking these results together, we have identified FUT8 as a key modulator of NK cell biology by regulating their development, IL-15R expression, and signaling. - Source: PubMed
Publication date: 2025/08/02
Sudholz HarrisonMeng XiangpengPark Hae-YoungShen ZihanNikolic IvaCursons JosephGoddard-Borger Ethan DSchuster Iona SAndoniou Christopher EDegli-Esposti Mariapia AScott Nichollas EChopin MichaelRautela JaiScheer SebastianHuntington Nicholas D - Here, we describe the use of a homologous knockin mouse model to further decipher the mechanism(s) of a novel human homozygous IL2RB hypomorphic mutation. Our model recapitulates the human immune dysregulation phenotype, showing decreased mutant interleukin-2Rβ (IL-2Rβ) cell-surface expression, impaired IL-2/15-dependent STAT5 signaling, elevated serum IL-2/15 levels, expanded effector memory CD8 T cells, and severely reduced regulatory T cells (Tregs). Using mixed bone marrow chimeras (BMCs) and wild-type (WT) Treg transfers, we distinguish receptor-intrinsic from receptor-extrinsic immunopathogenesis. Both approaches suppress abnormal serum cytokine levels and autoimmunity without affecting endogenous mutant Tregs. Mutant animals receiving WT Tregs neonatally exhibit almost complete restoration of conventional T cell distribution, IL-2Rβ receptor surface expression, and STAT5 signal transduction, while BMC animals exhibit only partial restoration. Our findings demonstrate that CD8 T cells and Tregs have distinct IL-2/15 ligand/receptor ratios and signaling thresholds required for proper development/function, revealing mechanistic insights applicable to immunotherapy for autoimmunity. - Source: PubMed
Publication date: 2025/06/25
Cabrera-Martinez BereniceGarcia-Perez Josselyn EBaxter Ryan MLui Victor GGhosh TusharkantiEken AhmetKostka-Newman ZanderGarcia John Rhey MharRahkola JeremyGessner Rachel LDutmer Cullen MKlarquist JaredPietras Eric MGhosh DebashisJohnson Sara AKedl Ross MHsieh Elena W Y - Seasonal allergic rhinitis (SAR) is a prevalent inflammatory condition, yet its molecular mechanisms and reliable biomarkers remain incompletely understood. This study aimed to identify key inflammation-related proteins and pathways associated with SAR by investigating seasonal proteomic profile variations and their correlations with SAR symptoms. - Source: PubMed
Publication date: 2025/05/12
Shen JiaqiZheng XinliangYan MohanFeng MinqianDing ChanXie ShuanghuaXu Huadong