KLRG1 antibody (Azide Free)
- Known as:
- KLRG1 (anti-) (Azide Free)
- Catalog number:
- 10r-k107amsle
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- KLRG1 antibody (Azide Free)
Ask about this productRelated genes to: KLRG1 antibody (Azide Free)
- 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 antibody (Azide Free)
Related articles to: KLRG1 antibody (Azide Free)
- The major barrier to clinical translation of αCD137 immunotherapy is separating antitumor efficacy from hepatotoxicity driven by IFN-γ-producing CD8 T cells. We propose a strategy to limit toxicity by promoting contraction of excessively expanded CD8 T cells. We identify CD11cKLRG1 effector CD8 T cells (CD11cT) as the primary source of IFN-γ, recirculating between blood and secondary lymphoid organs (SLOs), where they undergo apoptosis during contraction. We show that lymphotoxin β receptor (LTβR) signaling restrains this contraction. Mechanistically, lymphotoxin-expressing B cells activate LTβR in fibroblastic reticular cells (FRCs), suppressing apoptosis of CD11cT cells in the spleen and sustaining their systemic circulation and liver infiltration. Pharmacological LTβR blockade abrogates hepatotoxicity by reducing the accumulation of IFN-γ-producing CD11cT cells while preserving tumor-specific CD8 T cell responses. These findings identify LTβR as a key regulator of effector CD8 T cell persistence and support the use of LTβR antagonists to improve the safety of αCD137-based immunotherapy. - Source: PubMed
Publication date: 2026/04/22
Shein Sergey AKorchagina Anna AWang Li-JuLai ZhaoChen YidongFisher Jacob SLudewig BurkhardLancaster Jessica NFu Yang-XinKoroleva EkaterinaTumanov Alexei V - There is growing evidence that neonates harbor innate-like CD8a T cell subsets that contribute to both protection and hyper-inflammatory states. It remains unclear, however, where these innate-like features are found among the many conventional and unconventional T cell populations that can upregulate the CD8 receptor. Further delineation of these unique populations and functions, with a focus on CD8ab co-expression, will enable studies that seek to understand the unique immune features in conventional T cell populations that are present during fetal and early postnatal life. We used cord blood from infants across the full viable gestational age range to examine phenotypic and transcriptional heterogeneity, with a particular focus on the naïve T cell pool. We report a set of fetally-derived and innate-like naïve CD8αβ T cells ('FITs') that are marked by their KLRG1 CD161 phenotype, unique transcriptomic features and which are sparsely detected in adult peripheral blood. Additionally, using T cell receptor repertoire profiling, we can distinguish FITs from well-described and semi-invariant unconventional T cell populations such as mucosa-associated invariant T cells. Our delineation of FITs' unique features will enable future investigation into their ontogeny and tissue distribution, and ultimately their role in immune-related outcomes in preterm infants. - Source: PubMed
Publication date: 2026/03/09
Geber AdamGroff BrandonMcMurry JordanLaniewski NathanTyrlik AdamKean ConnorWang RuoqiaoCastro-Melendez DarlineNarvaez-Miranda JaniretVance NataliePryhuber GloriaMosmann TimothyRudd Brian DThakar JuileeTopham David JGrimson AndrewScheible Kristin - Checkpoint blockade therapies have demonstrated clinical benefit across multiple cancer types; however, many patients with immune cell infiltration remain non-responsive or develop resistance. This suggests that additional, unidentified regulatory pathways limit treatment efficacy. The purpose of this study was to investigate the role of the inhibitory receptor KLRG1 in limiting antitumor immunity and to evaluate its potential as a therapeutic target in patients refractory to first-generation checkpoint inhibitors. - Source: PubMed
Publication date: 2026/04/09
Jones Tyler AndrewShapiro Jason WSinicrope StephenLi ShuyinYasuda KeiIovino MatthewSevere NicolasPinkas JanGajewski Thomas - - Source: PubMed
Publication date: 2026/02/20
Greenberg Steven A - Isocitrate dehydrogenase 1 (IDH1) mutations confer distinct biological properties to gliomas, including the reshaping of the tumor immune microenvironment. While T cell dysfunction in glioblastoma has been extensively characterized, the role of innate lymphoid cells (ILCs)-critical regulators of tissue homeostasis and early immune responses- remains poorly understood. - Source: PubMed
Publication date: 2026/04/01
Erdem SerifeHaliloglu YesimUslu Inayet NurHouran MohammadUlutabanca HalilVural AlperenErturhan Mehmet BeratCanatan HalitEken Ahmet