NCR1 (Natural Cytotoxicity Triggering Receptor 1)

As described herein, the finding that the mAb that recognizes sheep and cattle NKp46 recognizes the orthologue in goats has provided an opportunity to identify a subset of leukocytes with phenotypic and functional characteristics of NK cells in goats, a profile consistent with NK cell features reported in other animal species. The study expands opportunities to conduct comparative studies on NK cells across different species and underscores the potential use of goats as an animal model in investigating NK cell biology in health and disease.

In addition, we found that higher levels of DEPs, such as CD27, TNF, CCL3, CCL4, IL12RB1, PDCD1, and GZMB, in patients with genetic alterations associated with poor prognosis. Our Olink proteomics analysis identified nine key proteins that were differentially expressed between the pediatric B-ALL and control groups, which may contribute to the diagnosis and/or risk stratification of pediatric B-ALL.

Additionally, qRT-PCR experiment verified the differential expression of crucial genes in clinical AML samples. This study provides a promising immune-based prognostic model for AML, contributing to better patient stratification and personalized treatment approaches.

These findings establish UTY as a sex-specific epigenetic modulator that restricts NK cell maturation while promoting cytotoxic function. Our data further reveal a cooperative role for UTY and UTX in orchestrating NK cell development via transcriptional regulation.

In tumor-bearing mice, ACT using T cells treated ex vivo with DMOG and agonist antibodies resulted in decreased tumor growth compared to ACT using control T cells and increased intratumoral markers of CD8+ T cells (CD7, CD8A, and CD8B1), natural killer cells (NCR1 and KLRK1), and cytolytic activity (perforin-1 and tumor necrosis factor-α). Costimulatory receptor gene expression was also induced when CD8+ T cells were treated with three highly selective HIF stabilizers that are currently in clinical use.

Single-cell RNA sequencing (scRNA-seq) data also provided evidences that Prdm1 maintains functional subsets of cNK cells and liver ILC1s and facilitates communications between cNK cells, liver ILC1s, and macrophages. The present study unveiled a novel regulatory mechanism of Prdm1 in cNK cells and liver ILC1s, showing promising potential for developing innovative immune therapy strategies against liver cancer.

Here we propose a new robust approach for the identification of PB NK-cells, based on the combination of NKp80 plus CD16. However, in chronic lymphoproliferative disorders of NK-cells, addition of CD56 is recommended to identify clonal NK-cells, due to their frequent aberrant NKp80- phenotype.

Thus, increased pGSN expression suppresses the anti-tumor functions of NK cells. The study provides insights into why immunotherapy is rarely effective in patients with OVCA and suggests novel treatment strategies.

Splenectomy concurrently enhances T cell-mediated acquired immunity by reducing the number of monocytic MDSCs and suppresses innate immunity by decreasing the number of NK cells. Splenectomy has opposite effects on primary and metastatic lesions through differential regulation on these two immune systems.

This was marked by strongly elevated basal IL17A and IL17F expression and the secretion of IL-17. Together, our data present Kit225 cells as a valuable model for studying the interplay between cytokines and their contribution to T cell survival, proliferation, and differentiation.

Our preliminary data suggest that using EVs to treat tumors could potentially alter components of the immune system, which causes hyperactivation of specific cell types and can lead to aggressive growth. These data will guide the designing of new personalized diagnostic approaches based on in-depth study of the TME.

A single injection of NK-EVs resulted in tumour eradication in some but not all mice. Thus, chemotherapy-dependent tumour depopulation may create a unique window of opportunity for curative NK-mediated immunotherapy in GBM.