Ask about this productRelated genes to: SLAMF6 antibody
- Gene:
- SLAMF6 NIH gene
- Name:
- SLAM family member 6
- Previous symbol:
- -
- Synonyms:
- KALI, NTBA, KALIb, Ly108, SF2000, NTB-A, CD352
- Chromosome:
- 1q23.2-q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-10-29
- Date modifiied:
- 2018-02-13
Related products to: SLAMF6 antibody
Related articles to: SLAMF6 antibody
- T helper (Th) and T follicular helper (Tfh) cells support cellular and humoral immunity, respectively. How activated CD4 T cells commit to these fates remains unclear. Using a mouse vaccination model, we traced endogenous, polyclonal CD4 T cells during bifurcation into Th1 and Tfh lineages. We found that Th1 and Tfh cells originate from shared, highly proliferative TCF1SLAMF6PD-1 precursor clones that co-express Th1- and Tfh-related transcription factors and chemokine receptors, including T-bet, BCL6, CXCR3, and CXCR5. The generation of common Th1/Tfh precursors from naive CD4 T cells requires CD28 costimulation but occurs independently of CD40, ICOS, and interaction with type 1 conventional dendritic cells (cDC1s) or B cells. Lineage commitment subsequently diverges: differentiation into Th1 cells relies on CD40 costimulation and cDC1s, whereas differentiation into Tfh cells requires ICOS costimulation and B cells. Activated CD4 T cells thus give rise to a common Th1/Tfh precursor whose fate depends on interactions with distinct antigen-presenting cells. - Source: PubMed
Publication date: 2026/04/21
Bosma Douwe M TBusselaar JuliaStaal Mo Dde Koning MylèneReljić MirnaLei Xinde Wit TomXiao YanlingBorst JannieSalerno Fiamma - - Source: PubMed
Li BinZhong Ming-ChaoGalindo Cristian CamiloDou JiayuQian JinTang ZhenghaiDavidson DominiqueVeillette André - - Source: PubMed
- Type 1 diabetes (T1D) is a genetic autoimmune disease in children and young adults, with no cure, emphasizing the need for novel genetic-based therapies. Differential analysis using the "Limma" package identified 42 upregulated genes in the peripheral blood of T1D patients. Gene Ontology/Kyoto Encyclopedia of Genes and Genomes analysis suggested that CD38 may contribute to T1D development. LASSO (least absolute shrinkage and selection operator) machine learning successfully screened EMOES, SH2D1B, and TRDV3 from these upregulated genes. We selected SH2D1B, which is included in our natural killer cell-mediated cytotoxicity-related genes gene set, for further protein interaction network analysis, the analysis results revealed a highly correlated network of LY9, SH2D1B, CD244, and SLAMF6. Through immune infiltration analysis, we demonstrated resting natural killer (NK) cells and monocyte migration were upregulated, both were significantly related to the expression levels of LY9, SH2D1B, and CD244. Single-cell RNA sequencing analysis showed that both SH2D1B and CD244 were enriched in NK cells, and SH2D1B has the potential to modulate the function of NK cells. Subsequently, We performed gene set enrichment analysis with SH2D1B grouped into SH2D1Bhigh NK cells, SH2D1Blow NK cells, and SH2D1B- NK cells, which showed that the gene set related to the response to IFNγ is enriched in SH2D1Bhigh NK cells. With the analysis results, we performed differential expression analysis and validated the results by Western blotting. Finally, we identified activation of the IFNγ/JAK1/STAT/CD38 pathway in SH2D1Bhigh NK cells. Our findings suggest that SH2D1Bhigh NK cells may produce adenosine by IFNγ/JAK1/STAT/CD38, to limit autoimmunity and presumably disease development. - Source: PubMed
Chen JiahuiFu LinghuaGong YipengLiao LeYu WanqianYu PengXu GaosiYang Pingping - Inhibitory receptors like PD-1 and CTLA-4 contribute to T cell dysfunction in cancer. Monoclonal antibodies (mAbs) blocking the interactions in trans of these receptors with their ligands on cancer cells or in the tumour microenvironment lead to clinical responses in some but not all types of cancer. Signalling lymphocytic activation molecule 6 (SLAMF6, also known as Ly108) is a homotypic receptor preferentially expressed on progenitor or stem-like exhausted T (T) cells, but not on terminally exhausted T (T) cells, as demonstrated in mouse models. In contrast to T cells, T cells retain the capacity for functional restoration after immune checkpoint blockade. The role of SLAMF6 in T cells remains ambiguous, as it has both activating and inhibitory effects, complicating its evaluation as a therapeutic target. Here we find that SLAMF6 was triggered in cis by homotypic interactions at the T cell surface. These interactions elicited inhibitory effects that suppressed activation of T cells and limited anti-tumour immunity, independently of SLAMF6 expression on tumour cells. mAbs against human SLAMF6 with a robust ability to disrupt the cis interactions strongly augmented T cell activation, reduced the proportions of exhausted T cells and inhibited tumour growth in vivo. Collectively, these findings show that SLAMF6 functions exclusively as a T cell inhibitory receptor, which is triggered by cis homotypic interactions. They also position SLAMF6 as a promising target for therapies aimed at enhancing anti-tumour immunity, regardless of SLAMF6 expression on tumour cells. - Source: PubMed
Publication date: 2026/02/11
Li BinZhong Ming-ChaoGalindo Cristian CamiloDou JiayuQian JinTang ZhenghaiDavidson DominiqueVeillette André