CD208 LAMP3 antibody Ab host: Rabbit
- Known as:
- CD208 LAMP3 (anti-) Antibody production species: Rabbit
- Catalog number:
- 'C16533-1
- Product Quantity:
- 50 Вµg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- CD208 LAMP3 antibody host: Rabbit
Related genes to: CD208 LAMP3 antibody Ab host: Rabbit
- 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
- Gene:
- PPP1R18 NIH gene
- Name:
- protein phosphatase 1 regulatory subunit 18
- Previous symbol:
- KIAA1949
- Synonyms:
- phostensin
- Chromosome:
- 6p21.33
- Locus Type:
- gene with protein product
- Date approved:
- 2004-03-02
- Date modifiied:
- 2016-10-05
Related products to: CD208 LAMP3 antibody Ab host: Rabbit
Related articles to: CD208 LAMP3 antibody Ab host: Rabbit
- Type 1 conventional dendritic cells (cDC1s) are important for generating and sustaining antitumor immunity. Accordingly, the abundance of cDC1s in human tumors correlates with improved outcomes in cancer. Capitalizing on this role, we previously demonstrated that vaccination with murine cDC1s, generated in culture from bone marrow cells (termed here "in vitro-derived cDC1s"), elicits durable tumor control in multiple preclinical models; however, the immunological mechanisms underlying the efficacy of cDC1 vaccination remain unclear. Here, we examined whether in vitro-derived cDC1s resemble tumor-infiltrating DC populations and whether MHC-I and MHC-II antigen presentation contribute to cDC1-mediated tumor control following vaccination in melanoma. As expected, MHC-I or MHC-II deficiency had minimal impact on the transcriptional state of cDC1s in homeostasis or following stimulation with the adjuvant poly dI:dC. Moreover, in vitro-derived cDC1s cultured under steady-state conditions closely resembled tumor-infiltrating cDC1s, whereas their poly dI:dC-stimulated counterparts resembled CCR7+ tumor-infiltrating DC populations, also referred to as mregDCs or LAMP3+ DCs. Our data further show that both MHC-I and MHC-II contribute to tumor control upon cDC1 vaccination and that coexpression of MHC-I and MHC-II on the same cDC1 is necessary for a robust vaccine response. We also identified an important function for host cDC1s in supporting the efficacy of vaccination with in vitro-derived cDC1s, as judged by impaired tumor control in Irf8 + 32-/- mice, which lack endogenous cDC1s. Overall, these results indicate that effective antitumor responses depend on MHC-I and MHC-II antigen presentation by vaccine-delivered cDC1s, with additional contributions from host cDC1s. - Source: PubMed
Pineda Josué EMinowa TomoyukiShen LiZhou YifanDyevoich AllisonPatel BhaktiSchneider Sarah MKeshari SunitaSaha AkataRiba Morgan NWang JingWatowich Stephanie SGubin Matthew M - Primary cutaneous T-lymphomas (CTCL), particularly in their early stages, frequently present with clinical and histopathologic features that overlap with atopic dermatitis (AD) and psoriasis, contributing to diagnostic delay and ineffective, or even deleterious, treatment approaches. Thus, minimally invasive molecular tests capable of distinguishing CTCL from benign inflammatory dermatoses are urgently needed. - Source: PubMed
Publication date: 2026/08/07
Fleischli AbigailBar JonathanManson MeredithNg Brandon DMeledathu ShannonBurnett AmeliaChefitz GabriellaEstrada Yeriel DGour DigpalCices AhuvaCorrea da Rosa JoelBrunner Patrick MGuttman-Yassky Emma - CXCL13 T cells and LAMP3 dendritic cells (DCs) are pivotal players in orchestrating anti-tumor immune responses, particularly within tumor tertiary lymphoid structures (TLS). However, their heterogeneity, differentiation trajectories, and clinical relevance in bladder cancer remain incompletely defined. This study integrated single-cell RNA sequencing (scRNA-seq) data (16 bladder cancer patients, 113,905 post-quality-control cells) and spatial transcriptomics to characterize CXCL13 T cell/LAMP3 DC subsets, their differentiation pathways (via Velocyto trajectory analysis), and intercellular crosstalk (via receptor-ligand mapping). A risk model (DTscore) was constructed using marker genes of these cells and validated in the IMvigor210 (atezolizumab-treated bladder cancer) and TCGA-BLCA cohorts. scRNA-seq clustering identified 10 immune and 3 nonimmune cell types, with T cells stratified into 8 subpopulations (including CD4CXCL13 T cells and CD8CXCL13 T cells) and DCs into 9 subgroups (including LAMP3 DCs). Receptor-ligand mapping and spatial transcriptomics confirmed functional crosstalk between CXCL13 T cells and LAMP3 DCs via key pairs (e.g., CCR7-CCL19, CXCR5-CXCL13, PDCD1-CD274) within TLS. The DTscore was developed using 8 marker genes (TSHZ2, ALOX5AP, GADD45G, TXN, CHN1, CCL19, CXCL13, ICA1) and exhibited robust prognostic and predictive performance: In the IMvigor210 cohort, high DTscore correlated with significantly poorer overall survival (OS) and a 3.27-fold lower immunotherapy response rate (11% vs. 36%, p = 4.23e-07); multivariate Cox regression confirmed DTscore as an independent OS predictor (hazard ratio = 1.97, p < 0.001). DTscore retained prognostic value in TCGA-BLCA (OS: p = 0.003; disease-specific survival: p < 0.001) and effectively predicted atezolizumab response even in the "immune desert" phenotype (p = 0.04). Combining DTscore with tumor mutational burden/tumor neoantigen burden yielded an AUC of 0.8122 for response prediction. Additionally, high DTscore was associated with higher OS hazard ratios in patients with wild-type TTN, RB1, EP300, or FGFR3 (all p < 0.01), while FGFR3 mutations correlated with lower immune checkpoint/CXCL13 expression. This study delineates the heterogeneity and interactions of CXCL13 T cell/LAMP3 DC subsets in bladder cancer TLS and validates DTscore as a robust tool for predicting OS and immunotherapy response, offering a potential guide for personalized bladder cancer treatment. - Source: PubMed
Publication date: 2026/08/05
Zhou LinZhu JinchaoLiu YushanXu Bin - Immune checkpoint inhibitors now occupy a central place in the management of advanced gastric and gastroesophageal junction adenocarcinoma, yet durable benefit remains uneven across patients, lesions, and metastatic sites. Conventional biomarkers, including programmed death-ligand 1 scoring, microsatellite instability or mismatch-repair deficiency, HER2, claudin 18.2, Epstein-Barr virus status, and tumor mutational burden, define important clinical and biological contexts but do not fully explain whether antitumor immunity can reach, recognize, and control malignant tissue. This narrative Review uses a spatial immune-ecology lens to interpret immunotherapy resistance through three linked tissue-level axes: immune accessibility, immune competence, and immune suppression. Within this framework, gastric and gastroesophageal junction adenocarcinoma can be organized into immune-desert, immune-excluded, inflamed-dysfunctional, tertiary lymphoid structure-rich immune-active, and metastatic-niche ecosystems, with particular emphasis on peritoneal and liver metastases. We distinguish gastric or gastric/gastroesophageal junction immune-checkpoint-inhibitor outcome-linked evidence from gastric spatial-biology or prognostic evidence, pan-cancer mechanisms, and more exploratory concepts. For now, spatial features such as tumor-nest CD8+ infiltration, tertiary lymphoid structure maturity, LAMP3+ dendritic-cell proximity, cancer-associated fibroblast-myeloid barriers, and lesion-level biomarker discordance are best regarded as complements to guideline-supported biomarkers and as pharmacodynamic endpoints, rather than independent treatment-selection tools, until they are tested prospectively in gastric and gastroesophageal junction immune-checkpoint-inhibitor outcome-linked cohorts. - Source: PubMed
Publication date: 2026/07/21
Zhang XinriChen XingyuLeng Yan - Adverse historical conditions shape biodiversity by driving demographic shifts and genomic divergence through evolutionary mechanisms. Selective pressures foster adaptive strategies in response to extreme environments, with hibernation as a key example. The expression of torpor and its various forms exemplify such adaptations. However, the genomic basis of these processes and the influence of evolutionary forces, particularly natural selection, remain largely unexplored. The Monito del Monte (), a small marsupial considered a living fossil, exhibits torpor, hibernation, and aestivation as key survival strategies. In this study, we investigated genomic adaptations in and their potential relationship with the physiological state of torpor and hibernation. Historical climate change, along with varying expansions and bottlenecks, appears to have shaped the genetic diversity and local adaptation of . At the ancestral node, positive selection was detected in , and , alongside enrichment in the MAPK signaling and steroid hormone biosynthesis pathways-both previously implicated in hibernation physiology. Gene family expansions further converged on mitochondrial maintenance and redox regulation. At the species level, and show no overlap in positively selected genes: presents additional signals in LSS and RASL11B, related to sterol and stress-response metabolism, while shows signatures of broad thermal stress tolerance through HSPA2. These findings underscore unique adaptations possibly linked to hibernation in and species-specific differences. - Source: PubMed
Publication date: 2026/08/02
Gonzalez-Ugalde ElisaAvendaño Paula MQuintero-Galvis Julián FPizarro Eduardo JCubillos Francisco ANespolo Roberto FLeón FabiolaVianna Juliana A