CD1C (CD1c Molecule)

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.

Despite the small sample size and absence of functional experiments, our results suggest that Pazopanib promotes cytotoxic immune programs but, by six months, reprograms PLT-EVs towards different adhesion characteristics contributing to Treg and MDSC expansion while suppressing NK activity. PLT-EVs may influence the balance between immune activation and suppression during anti-angiogenic therapy, suggesting PLT-EVs as biomarkers and therapeutic targets in mRCC.

Spatially resolved single-cell transcriptomic and immunohistofluorescence analyses of human carcinomas demonstrated that lymphocytes and most DCs were enriched within the tumor stroma, while CD207+ DCs were mostly embedded within tumor nests. These DC-VERSEs provide a robust resource available to the scientific community on DCs in health and pathology.

Using two independent datasets (GSE249956 and GSE98206), differentially expressed genes (DEGs) were identified between ibrutinib-resistant and sensitive CLL samples. In the broader context, PD-1 expression in CLL cells is linked to active proliferation and immune escape. Overall, our findings emphasize PDCD1's central role in ibrutinib resistance through immune checkpoint pathways and support the rationale for combining BTK inhibitors with immune checkpoint blockade therapies in resistant CLL cases.

It also significantly affects the frequency of vLC- and CD1c+CD14- vDC-induced IL - 10+ and IL - 21+CD4+ T cells. This study provides new insights into the immunological landscape of the human VM tissues, with implications for the development of targeted immunomodulatory strategies at this mucosal site.

scRNA-seq identified the intricate tumor immune microenvironment, highlighting the pivotal roles of TAMs and mast cells in gastric cancer peritoneal metastasis. The CCL5-CCR1 pathway emerged as a potential immune checkpoint, offering novel insights for future immunotherapeutic and targeted therapeutic strategies in the treatment of gastric cancer peritoneal metastasis.

Notably, distinct molecular subtypes were associated with specific changes in the immune landscape, with the most significant changes observed in the triple-negative subtype. Our data indicate that the systemic immune landscape undergoes more profound alterations in metastatic breast cancer than non-metastatic cases, with disease stage exerting a greater influence on systemic immune composition than tumor subtype.

Our findings deeply decipher the heterogeneous TMEs between IM and MO, which provide a comprehensive landscape of multifocal HCC.

We performed scRNA-seq, scTCR-seq, and scBCR-seq on 174,223 cells from 27 samples (22 paired pre- and post-treatment tumors, 2 unpaired tumors, and 3 adjacent tissues) treated with neoadjuvant camrelizumab (anti-PD-1) plus chemotherapy...This study reveals the cellular and molecular reprogramming of the TME during ICB therapy and identifies biomarkers of response and resistance in ESCC. These insights could potentially guide patient stratification and the development of targeted strategies to overcome ICB resistance.

The bispecific molecule induced potent re-directed T cell killing of CD1c positive cell lines. These proof-of-concept findings demonstrate that CD1c targeting TCR bispecific engagers might be good candidates for the development of non-MHC restricted, universal therapeutics for the treatment of CD1c+ leukemias.

Our findings provide a high-resolution resource for BC, elucidating the functional myeloid cell states, including TREM2+ macrophages, CMA1+ mast cells, and CD1C+ DCs. Furthermore, our study demonstrates that TREM2 and APP function as immune-modulating molecules, with potential therapeutic implications in the context of bladder cancer.

The increased expression of gene signatures formed by these transcripts resulted in a better prognosis in a set of patients with different tumors treated with anti-PD1 therapies, including 21 non-small cell lung cancers. We evaluated genomic alterations and transcriptomic patterns of SMARCA4 alterations in NSCLC tumors, identifying a relevant immunologic downregulated gene set linked with antigen presentation that predicts response to anti-PD1 therapies.