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
- Prostate cancer kills ≈350,000 yearly. While localized cases have 99% five-year survival, metastatic prostate cancer is hard to treat, with few options for tumors resistant to androgen deprivation. To leverage the immune system to fight prostate cancer, we developed a non-integrative lentiviral vector, namely "Lenti-PROST-02", which encodes clusters of T cell immunodominant regions of human prostatic acid phosphatase and prostate-specific antigen. Immunotherapy with Lenti-PROST-02 in a preclinical virulent prostate tumor model resulted in complete tumor eradication in vast majority of the treated animals. This antitumor effect was concomitant with induction of poly-functional CD8 T splenocyte effectors against numerous T cell epitopes of the antigens encoded by Lenti-PROST-02, increased proportions of tumor-infiltrating CD8 T cells with activated/differentiated/effector phenotype and a "cold-to-hot" inflammatory switch of the tumor microenvironment. Immunity induced by Lenti-PROST-02 was long-lasting and prevented tumor relapse. It was characterized by the persistence of CD44 CD62L CD127 KLRG1 CD8 memory T cells in secondary lymphoid organs, as well as an antigen-diversified memory response. Therefore, Lenti-PROST-02 therapeutic vaccine is a promising approach for prostate immuno-oncotherapy. - Source: PubMed
Publication date: 2026/07/18
Vesin BenjaminFert IngridCiret SylvainDouguet LaëtitiaMoncoq FannyNoirat AmandineAuthié PierreLe Chevalier FabienNevo FabienBlanc CatherineNemirov KirillMajlessi LalehCharneau Pierre - Mitochondria activate immunity, but the role in cancer is unknown. Here, we report that transgenic expression of Parkin, a regulator of mitochondrial fitness, induces inflammation and interferon (IFN) gene signatures, suppresses prostate cancer formation and generates CD8 and CD20 intraprostatic immune aggregates. These had hallmarks of mature tertiary lymphoid structures (TLS), expressing markers of B cell maturation (CXCL13, CCL21), germinal center formation (BCL6, GL7), mature dendritic cells (MHC-II/CD208) and high endothelial venules (LYVE-1). Parkin TLS showed high Ig gene expression, recruitment of CXCR5 follicular T helper cells and expansion of CD69/KLRG1 effector T cells. Conditioned medium from Parkin-positive cells expanded memory B and plasma cells, increased IgG1 production, and sustained B and T cell migration. Finally, conditional expression of Parkin induced TLS formation, upregulated Ig chains and inhibited prostate cancer growth, in vivo, whereas Parkin reconstitution in IFNAR1, CD8 or CD20 knockout mice had no effect. Therefore, mitochondrial immunity orchestrates antitumor responses, and TLS formation contributes to tumor suppression. - Source: PubMed
Publication date: 2026/08/07
Perego MichelaKossenkov Andrew VGhosh Jagadish CCamisaschi ChiaraTursi Nicholas JWeiner David BAltieri Dario C - Immune evasion remains a major barrier to effective immunotherapy in cancer. Coordinated activation of different immune cell types shapes immune responses within the tumor microenvironment (TME). In this study, we uncovered a spatiotemporal synergy between cytotoxic T lymphocytes (CTL) and natural killer (NK) cells in tumors with low T-cell infiltration. An integrative multiomics approach combining spatial transcriptomics, single-cell RNA sequencing, and high-dimensional flow cytometry demonstrated that vaccination, capable of activating both innate and adaptive immunity, rapidly reshapes the TME. Early infiltration of IRF8+KLRG1+ NK cells established a chemokine-rich niche together with myeloid cells that promoted the recruitment of antigen-primed CXCR3+ CTLs. The accompanying inflammatory monocyte recruitment and dendritic cell activation led to the coordinated structural and chemotactic remodeling of the TME. Functionally, NK-CTL clustering at the tumor margin was associated with enhanced cytotoxic activity and sustained immune engagement. These spatially organized immune interactions involved CCR5-CCL5 and CXCR3-CXCL9 signaling pathways that coordinate communication between innate and adaptive immune compartments. Together, these findings reveal a previously unrecognized NK-CTL cooperative program that promotes the transition of poorly infiltrated tumors toward an inflamed, immune-responsive state. More broadly, this study illustrates how spatially resolved multiomics approaches can uncover immune interactions and provides a conceptual framework for designing next-generation immunotherapies that mobilize coordinated innate and adaptive immunity. - Source: PubMed
Publication date: 2026/08/03
Shimizu KanakoSanpei AnLiu YanIshibashi TakuyaYanagawa MarinNakazato HiroshiShinga JunUeda ShogoYamasaki SatoruFujii Shin-Ichiro - Systemic lupus erythematosus (SLE) is a heterogeneous autoimmune disease characterized by loss of immune tolerance and multi-organ inflammation. Although its pathogenesis involves multiple factors, the peak incidence of SLE in individuals over 48 years of age points to immunosenescence as a key driver of the disease.Even in younger patients, SLE frequently often presents as premature aging of the immune system. This review synthesizes recent advances in understanding how immunosenescence drives pathogenesis through immune dysregulation across major lymphocyte and myeloid subsets. Within the chronic inflammatory microenvironment, replicative exhaustion of T cells leads to accelerated telomere attrition, persistent activation of the DNA damage response, and telomerase dysfunction. This cascade culminates in the accumulation of senescent T cells displaying a characteristic CD28CD57KLRG1 phenotype, accompanied by a pro-inflammatory state defined by enhanced cytotoxicity and impaired regulatory function. These characteristics correlated directly with disease activity and cumulative organ damage. The process arises from the interplay of metabolic reprogramming and epigenetic remodeling. In parallel, age-associated B cells (ABCs) accumulate, producing high-affinity anti-dsDNA and other autoantibodies, and potentiating inflammation via enhanced antigen presentation. Meanwhile, an aged bone-marrow microenvironment together with clonal hematopoiesis skews monocyte and macrophage polarization toward a pro-inflammatory (M1) profile. These cells show reduced phagocytic capacity and heightened secretion of senescence-associated secretory phenotype (SASP)-like mediators, further driving inflammaging. This review synthesizes current insights into the relationship between SLE risk and immunosenescence. We discuss the mechanisms through which immune aging instigates autoimmunity and explore emerging therapeutic strategies aimed at mitigating immunosenescence. - Source: PubMed
Publication date: 2026/07/31
Jiang XiaojingLiang ZiqianZhao ChaoranLi FangSu QinyiWang YanZhang ShengxiaoCheng Ting - (Mtb) remains the leading cause of death from a single infectious agent. Although BCG protects against disseminated tuberculosis in infants, it has failed to curb transmission among adults. Animal models are used to prioritize vaccines entering clinical trials, but current models use Mtb-naïve mice, limiting their relevance to humans in endemic settings, the primary targets of vaccine trials. Here we used a mouse model of Mtb exposure, CoMtb, where a cervical lymph node Mtb infection protects against aerosol challenge, consistent with historical observations in humans that prior Mtb exposure reduces disease risk. When we compared the impact of CoMtb on vaccine efficacy, BCG failed to provide added protection over CoMtb, while protein subunit vaccination further reduced lung burdens. This protection was associated with decreased KLRG1+ vascular CD4+ T cells and enhanced polyfunctional lung CD4+ T cells before and after aerosol challenge. Our findings were corroborated in an analysis of vaccinated humans stratified by QuantiFERON-TB status, which revealed a similar enrichment of polyfunctional CD4+ T cells in Mtb-exposed individuals. These data support the use of CoMtb to test vaccine efficacy in Mtb-exposed individuals and highlight the potential of subunit vaccines in endemic regions. - Source: PubMed
Publication date: 2026/07/16
Cohen Sara BWoodworth Joshua SLindenstrøm ThomasGela AneleDuffy Fergal JAitchison John DScriba Thomas JNemes ElisaMortensen RasmusUrdahl Kevin B