KLRG1
- Known as:
- KLRG1
- Catalog number:
- Y214308
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- KLRG1
Related genes to: KLRG1
- Gene:
- KLRG1 NIH gene
- Name:
- killer cell lectin like receptor G1
- Previous symbol:
- -
- Synonyms:
- MAFA, 2F1, MAFA-L, CLEC15A
- Chromosome:
- 12p13.31
- Locus Type:
- gene with protein product
- Date approved:
- 1999-09-17
- Date modifiied:
- 2016-01-14
Related products to: KLRG1
Related articles to: KLRG1
- Colonic immune homeostasis is critically maintained by regulatory T (Treg) cells. Here, we identify SUMO-specific peptidase 1 (SENP1) as an important regulator of colonic Treg function and intestinal immune homeostasis. Treg-specific Senp1 deletion does not impair thymic Treg development, but selectively disrupts the homeostasis of colonic Treg subset without affecting Treg maintenance in other peripheral tissues. Mechanistically, SENP1 deficiency reduces CD25 expression on Tregs, blunting IL-2 responsiveness and compromising their expansion and survival. This is associated with a selective reduction in the proportion of tissue-adapted Gata3 Tregs and accumulation of CD25 precursor-like Tregs in the intestinal lamina propria. Senp1 depletion also downregulates core effector Treg signature genes including Gata3, Klrg1, and Il1rl1, correlating with dysregulated Th2 response control. Single-cell RNA sequencing analysis reveals transcriptional alterations consistent with impaired colonic Treg tissue adaptation after SENP1 ablation. Functionally, with adoptive transfer experiments we found that Senp1-deficient Tregs show impaired accumulation in vivo and are associated with weaker control of pathogenic T cell expansion in the colon. Consistently, Treg-specific Senp1-deficient mice display heightened susceptibility to DSS-induced colitis, highlighting a critical role of SENP1 in sustaining functional Treg programs and limiting pathogenic intestinal inflammation. - Source: PubMed
Publication date: 2026/05/16
Hao YanyunLiu HongzhiLiang QiuliFan QiujuWang TianshiCheng Jinke - Antiretroviral therapy (ART) has significantly extended the life expectancy of people with HIV (PWH), rendering population ageing and immunosenescence prominent clinical priorities. T-cell senescence is linked to mitochondrial dysfunction and drives age-related immune remodelling, yet how HIV infection and ageing jointly shape CD4 and CD8 T-cell immunophenotypes and mitochondrial remodelling remains unclear. This cross-sectional study included 61 PWH on suppressive ART for ≥12 months and 61 age- and sex-matched HIV-negative men who have sex with men, stratified into younger (≤ 35 years) and older (≥ 50 years) groups. Multiparameter flow cytometry was used to profile CD4 and CD8 T-cell differentiation, stemness, activation/exhaustion, and metabolic phenotypes, together with mitochondrial mass and membrane potential. We found that ageing and HIV infection were associated with T-cell remodelling, characterized by expanded late-differentiated phenotypes and reduced stem-like, homeostatic and costimulatory CD4 and CD8 T-cell subsets, as indicated by upregulated CD57 and CX3CR1 and downregulated CD45RACD31, FOXO1, and CD28. Notably, younger PWH had an ageing-like CD4 T-cell profile, with higher CD57, CX3CR1 and TIGIT expression than younger HIV-negative individuals. In contrast, HIV-related CD8 T-cell perturbations (KLRG1, NKG2C and CD95) were more pronounced in older PWH. PWH exhibited increased mitochondrial mass and membrane potential in both total and senescent-like CD4 and CD8 T cells, particularly in CD8 T cells from older PWH. In CD4 T cells, KLRG1 and CX3CR1 expression correlated positively with age, and inversely with CD4 T-cell counts and CD4/CD8 ratio. By contrast, FOXO1 expression in CD8 T cells was inversely associated with age, late-differentiation markers, and ART duration in PWH. Overall, age is a major driver of T-cell immunosenescence, and HIV infection modulates and exacerbates these alterations. Mitochondrial stress, FOXO1 downregulation and immune network remodelling support a multifaceted model of HIV-associated immune ageing that may contribute to heterogeneous immune reconstitution in PWH, highlighting potential targets to mitigate immune ageing. - Source: PubMed
Publication date: 2026/05/14
Jin JunyanZhang XinXu QianqianXia WeiYan HongxiaWu HaoMoog ChristianeZhang TongSu Bin - NK cells are the core cells of the innate immune system, which can kill cancer cells non-specifically and almost do not cause immune rejection or neurotoxicity, thereby enabling broad application in immune cell therapy. The KLRG1/Cadherin signaling axis has been reported to inhibit the anti-tumor response of NK cells. However, the mechanism by which KLRG1 regulates CAR NK cell function remains unclear. - Source: PubMed
Publication date: 2026/05/14
Chen YiranFarooq Muhammad AsadHui XinhuiHuang YunheHu YueXue MinAjmal IqraRen YaojunJi YuzhouWang ChenJiang Wenzheng - We aimed to study the serologic, genetic, and immunologic underpinnings associated with cytotoxic T lymphocytes (CTLs) in rheumatoid arthritis (RA), using T-large granular lymphocytic leukaemia with comorbid RA (T-LGLL/RA) as a model of CTL-linked RA. - Source: PubMed
Publication date: 2026/05/12
Ananth KusumaMoosic Katharine BGomez-Banuelos EduardoWang HongTrejo-Zambrano IsabelJohnson RamonaKirschmann Jessica MarieDeddens TessElghawy OmarShemo BrynaRobinson William HKimpel DonaldBingham Clifton OFeith David JAntiochos BrendanAndrade FelipeLoughran Thomas PDarrah Erika - In multiple sclerosis (MS), T cells could contribute to disease in their attempt to control the Epstein-Barr virus (EBV). Here, we compared the presence of HLA-B7 (higher MS risk) or HLA-A2 (lower MS risk) and investigated the effector phenotype of EBV epitope-specific CD8 T cells in MS using spectral flow cytometry. In contrast to HLA-A2, HLA-B7-restricted CD8 T cells recognized few EBV epitopes. These HLA-B7-restricted EBV-specific CD8 T cells expressed CNS residency markers and were most abundant in postmortem CNS compartments of an HLA-A2B7 MS donor. HLA-B7-restricted EBV-specific CD8 T cells displayed a more exhausted phenotype (PD-1CD244CD160KLRG1TIGIT). In line with these findings, anti-EBNA1 IgG levels were elevated in patients with MS carrying HLA-B7 but lacking HLA-A2. These data support a model in which the confined response against EBV generates circulating HLA-B7-restricted CD8 T cells less able to control EBV and more prone to infiltrate the CNS. - Source: PubMed
Publication date: 2026/04/15
Reijm SanneMarques Ana MRip JasperCorsten Cato E AWierenga-Wolf Annet Fde Wit HarmMelief Marie-Josévan Hasselt Yifanvan Langelaar JamieNeuteboom RinzeWokke Beatrijs H AMueller Yvonne MSmolders Joostvan Luijn Marvin M