LAMP3 (Lysosomal Associated Membrane Protein 3)

In vitro -generated cDC1s resemble intratumoral DC populations found in mice and humans. MHC-I and MHC-II antigen presentation by vaccine-delivered cDC1s contribute to antitumor efficacy.Coexpression of MHC-I and MHC-II on the same cDC1 enhances vaccine responses.Antitumor responses reflect the activity of vaccine and endogenous cDC1s.

This mantle zone disorganization was associated with increased spatial niches involving Tregs, CD68+ CD163⁺ TIM3⁺ Macrophages, CD163⁺ TIM3 dim Monocytic-Myeloid Derived Suppressor Cells (M-MDSC), plasma B cells, and a decrease in spatial niches involving CD4⁺ T helper cells and fibroblastic reticular cells (FRCs). Together, our findings reveal parallel alterations in humoral and cell-mediated immunity within the regional LNs of patients with aggressive NSCLC.

Within it, we observe associations between naive T cell abundance and T cell activation-associated pathways, and correlations exist between distribution patterns of different lymphocytes and two transcriptomically distinct groups - more activated lymphocytes reside in the adjacent cancerous regions of Group A, while more resting lymphocytes settle in those of Group B. Within Group A, PD1+CD27+ CD8 T cells cluster in closer proximity to CD70+LAMP3+ dendritic cells. Our study unveils the gastric cancer tumour microenvironment at a spatial resolution and provides insights into the exploration of immunotherapy biomarkers.

In summary, we demonstrate that protein profiling of EVs in relation to osimertinib refractoriness has the potential to identify possible biomarkers that can indicate osimertinib treatment resistance, for example, CSPG4, HSPG2, TAGLN, TNC, THBS1, ANXA1 and CD73/NT5E. Studies in expanded cohorts should be conducted to further validate these putative osimertinib biomarkers.

We outline current and emerging myeloid-reprogramming strategies-including PI3Kγ and CSF1-CSF1R targeting, TREM2 antagonism, COX-2-PGE2 blockade, and adenosine-axis inhibition-and their integration with PD-(L)1 therapy, alongside single-cell/spatial endpoints to quantify on-treatment remodeling. The purpose of this mini-review is to provide a mechanistic and technology-informed framework to reference rational trial design and clinical translation for overcoming checkpoint resistance in CRC.

Our 9-LRG panel is a promising classifier for assessing the prognosis of BRCA. Notably, targeting EIF4EBP1 could potentially serve as a theoretical foundation for enhancing the prognosis of BRCA patients.

This study provides the first detailed mapping of CD1a+ and CD208+ DCs across NAM, pCRC and paired LM, indicating that their prognostic impact is determined not only by absolute numbers but, more importantly, by compartmental distribution and the temporal pattern of metastasis.

Multimodal cell-cell interaction analysis and functional experiments demonstrate that HEV expressed VCAM1 and ICAM1 recruits and activates CXCL13+ TLC through the CXCL13-ACKR1 pathway, which promotes TLS formation via CXCL13-CXCR5-dependent crosstalk with B lymphocytes. We further develop a single-cell/spatial TLS signature that captures the cellular ecosystem of iTLS-containing tumor, demonstrating predictive value for immunotherapy outcomes in GC patients.

This study identifies glycosylation-related gene candidates and establishes a preliminary diagnostic model for SLE, utilizing integrated bioinformatics analysis and experimental validation. These findings provide foundational insights for further exploration of SLE's molecular mechanisms and diagnostic advancement.

This study highlights key cellular and molecular mechanisms underlying bladder cancer progression Post-BCG treatment. Through single-nucleus RNA sequencing, we identified critical TME subtypes, TGF-β signaling involvement, and crucial ligand-receptor interactions such as DSC2-DSG2 and ENG-BMPR2, which may serve as preliminary biomarkers requiring confirmation in larger independent cohorts. These findings offer valuable insights into enhancement of treatment strategies and patient outcomes.

LAMP3⁺ dendritic cells (DCs) play a pivotal role in suppressing TLS formation, with IRF8 as a key transcriptional regulator, which may ultimately affect therapeutic response. These findings suggest early-Tex cells and modulation of TLS by LAMP3⁺ DCs can serve as indicators for optimizing neoCRT in MSS LARC.