Ask about this productRelated genes to: LAMP3 antibody
- Gene:
- LAMP3 NIH gene
- Name:
- lysosomal associated membrane protein 3
- Previous symbol:
- -
- Synonyms:
- LAMP, TSC403, DC-LAMP, DCLAMP, CD208
- Chromosome:
- 3q27.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-29
- Date modifiied:
- 2016-10-05
Related products to: LAMP3 antibody
Related articles to: LAMP3 antibody
- Laryngeal squamous cell carcinoma (LSCC) is typically diagnosed at advanced stages, highlighting the critical need for early intervention. By integrating single-cell and bulk RNA-seq data from LSCC, vocal cord leukoplakia (VCL), and LSCC precursors, we characterized dynamic remodeling of the tumor microenvironment during LSCC pathogenesis. We identified transcriptional program gene modules that reflect malignant epithelial cells (maEpCs). The infiltration of POSTN fibroblasts progressively increases from normal tissue to VCL and further to LSCC, accompanied by enhanced intercellular communication. These fibroblasts interact with maEpCs and endothelial cells via ligands such as MIF, promoting epithelial-mesenchymal transition, cancer stemness, and angiogenesis. Blocking MIF reversed cancer-associated fibroblast-driven invasion and angiogenesis. Here, we further revealed that an immunosuppressive microenvironment arises as early as the precancerous stage, with VCL exhibiting CD8 T cell exhaustion and abundant LAMP3 dendritic cells that correlate positively with Tregs and exhausted CD8 T cells, promoting early immune escape. Additionally, LSCC was uniquely enriched for a pro-tumor SPP1 macrophage subset with low phagocytic activity and high angiogenic potential, linked to poor prognosis. Our findings uncover key mechanisms driving LSCC malignant progression, offer insights for early diagnosis and prognosis assessment, and highlight MIF as a promising therapeutic target. - Source: PubMed
Publication date: 2026/03/28
Cai ZhimouLi YunZhang JinhongLuo ShiyunQiang ZhiweiLu ZhaoyueChen LinLei Wenbin - Breast cancer brain metastasis (BCBrM) remains one of the most lethal manifestations of breast cancer. Its response to immunotherapy is severely limited by the blood-brain barrier, which restricts immune cell infiltration and antigen presentation, thereby creating an immunosuppressive microenvironment. To overcome these barriers, recent studies have focused on novel immune checkpoints, including the Lymphocyte-Activated Gene 3-Galectin 3 (LAG3-LGALS3) and T-Cell Immunoreceptor with Ig and ITIM Domains-Nectin Cell Adhesion Molecule 2 (TIGIT-NECTIN2) axes, as well as on the reprogrammed metastatic ecosystem driven by immunosuppressive cells such as Forkhead Box P3-positive (FOXP3⁺) Regulatory T (Treg) cells, Lysosomal-Associated Membrane Protein 3-positive (LAMP3⁺) tolerogenic dendritic cells (DCs), C-C Motif Chemokine Ligand 18-positive (CCL18⁺) M2-like macrophages, Regulator of G-Protein Signaling 5-positive (RGS5⁺) cancer-associated fibroblasts (CAFs), Galectin 1-positive (LGALS1⁺) and TANK-Binding Kinase 1-positive (TBK1⁺) microglia, and phosphorylated Signal Transducer and Activator of Transcription 3-positive (pSTAT3⁺) reactive astrocytes. In addition, targeted inhibition of tumor-derived N-acetyltransferase 8-like (NAT8L) and metabolites N-Acetylaspartate (NAA), suppression of the N-Methyl-D-Aspartate Receptor (NMDAR) signaling pathway in tumor cells, and interventions against γ-Aminobutyric Acid (GABA)ergic reprogramming in BCBrM cells. Moreover, targeted interventions against distinct immune escape pathways-such as the Ubiquitin-Conjugating Enzyme E2T (UBE2T)/Cell Division Cycle 42 (CDC42)/Cluster of Differentiation 276 (CD276) and C-C Motif Chemokine Ligand 2-C-C Motif Chemokine Receptor 2/C-C Motif Chemokine Receptor 4 (CCL2-CCR2/CCR4) axes-have shown promise in reshaping the immune microenvironment and enhancing the efficacy of conventional immunotherapy. Collectively, this perspective outlines evolving strategies in immune checkpoint modulation, cellular ecosystem reprogramming, and neuroimmune intervention, providing a forward-looking framework to enhance the efficacy of immunotherapy in BCBrM. - Source: PubMed
Publication date: 2026/04/02
Zou YutianWu JiadiYuan ZeHe XiaofangTang Hailin - Nemolizumab reduces pruritus and skin lesions in patients with atopic dermatitis (AD), yet some patients develop cutaneous adverse events (CAEs) with increased serum thymus- and activation-regulated chemokine (TARC); mechanisms are unclear. - Source: PubMed
Publication date: 2026/03/12
Honryo AkiraMasuda ToshihiroNakamizo SatoshiTakafuji TakuyaMinami FuukaYonekura SatoruUchibayashi MidoriInoue KenichiKiyonari HiroshiYamanaka MasafumiIrie HiroyukiNakashima ChisaNakajima SaekoOtsuka AtsushiAsahina RyotaKabashima Kenji - The development of food-compatible strategies represents a critical advancement for the cryopreservation of aquatic biomaterials. This study evaluated the efficacy of food-grade fish oil (FO) as a synergistic adjunct within a standard DMSO-based cryomedium. Supplementation with 0.1% FO significantly increased the post-thaw viability of fish ovarian cells from 63.52% to 78.25% compared to the control (n = 6 biological replicates). Ultrastructural and functional analyses confirmed that FO treatment effectively maintained mitochondrial integrity (n = 3) and membrane potential (n = 6). Furthermore, FO supplementation mitigated oxidative stress by lowering MDA levels and modulating the expression of stress-response genes, specifically downregulating hsp70 and lamp3 (n = 6). Crucially, functional recovery was demonstrated by a shortened population doubling time (206.71 h, n = 6) and a 36.67% engraftment efficiency in a xenotransplantation model (n = 3). These findings establish FO as a potent, food-compatible supplement for optimizing conventional cryopreservation protocols in biotechnology. - Source: PubMed
Publication date: 2026/02/27
Yao JingtingLiu YihanXu HongyanSu Shengqi - COVID-19 can have diverse clinical manifestations, ranging from asymptomatic infection to critical illness with multiorgan involvement. While many patients recover fully, others develop long-COVID, a heterogeneous condition marked by persistent symptoms beyond the acute phase. The immunological pathomechanisms between long-COVID and other post-acute recovery states remain unclear. - Source: PubMed
Publication date: 2026/02/27
Meyer FranziskaTraidl StephanAmeri MiladDreher AnitaAbu-Rashed-Kufs NevineVontobel JanMöhrenschlager MatthiasDuchna Hans-WernerSandberg FeliciaBrüggen Marie-Charlotte