Transcriptomic landscapes of STING-mediated DNA-sensing reveal cellular response heterogeneity.

Transfection of plasmid DNA (pDNA) encoding target genes is a routine tool in gene function studies and therapeutic applications. However, nucleic acid-sensing-mediated innate immune responses influence multiple intracellular signaling pathways. The stimulator of interferon genes (STING) is a crucial adapter protein for DNA sensors in mammalian cells.

B7H6 is the predominant activating ligand driving natural killer cell-mediated killing in patients with liquid tumours: evidence from clinical, in silico, in vitro, and in vivo studies.

Background: Natural killer (NK) cells are a subset of innate lymphoid cells that are inherently capable of recognizing and killing infected or tumour cells. This has positioned NK cells as a promising live drug for tumour immunotherapy, but limited success suggests incomplete knowledge of their killing mechanism. NK cell-mediated killing involves a complex decision-making process based on integrating activating and inhibitory signals from various ligand-receptor repertoires.

FTO negatively regulates the cytotoxic activity of natural killer cells.

N -Methyladenosine (m A) is the most abundant epitranscriptomic mark and plays a fundamental role in almost every aspect of mRNA metabolism. Although m A writers and readers have been widely studied, the roles of m A erasers are not well-understood. Here, we investigate the role of FTO, one of the m A erasers, in natural killer (NK) cell immunity.

The Role of IL-7 and IL-7R in Cancer Pathophysiology and Immunotherapy.

Interleukin-7 (IL-7) is a multipotent cytokine that maintains the homeostasis of the immune system. IL-7 plays a vital role in T-cell development, proliferation, and differentiation, as well as in B cell maturation through the activation of the IL-7 receptor (IL-7R). IL-7 is closely associated with tumor development and has been used in cancer clinical research and therapy.

Tryptophanyl-tRNA Synthetase as a Potential Therapeutic Target.

Tryptophanyl-tRNA synthetase (WRS) is an essential enzyme that catalyzes the ligation of tryptophan (Trp) to its cognate tRNA during translation via aminoacylation. Interestingly, WRS also plays physiopathological roles in diseases including sepsis, cancer, and autoimmune and brain diseases and has potential as a pharmacological target and therapeutic. However, WRS is still generally regarded simply as an enzyme that produces Trp in polypeptides; therefore, studies of the pharmacological effects, therapeutic targets, and mechanisms of action of WRS are still at an emerging stage.

miR-150-Mediated Foxo1 Regulation Programs CD8 T Cell Differentiation.

MicroRNA (miR)-150 is a developmental regulator of several immune-cell types, but its role in CD8 T cells is largely unexplored. Here, we show that miR-150 regulates the generation of memory CD8 T cells. After acute virus infection, miR-150 knockout (KO) mice exhibited an accelerated differentiation of CD8 T cells into memory cells and improved production of effector cytokines.

MicroRNA-150 controls differentiation of intraepithelial lymphocytes through TGF-β receptor II regulation.

Background: Intraepithelial lymphocytes (IELs) in the intestines play pivotal roles in maintaining the integrity of the mucosa, regulating immune cells, and protecting against pathogenic invasion. Although several extrinsic factors, such as TGF-β, have been identified to contribute to IEL generation, intrinsic regulatory factors have not been determined fully.

Objective: Here we investigated the regulation of IEL differentiation and the underlying mechanisms in mice.

MicroRNA-150 modulates intracellular Ca levels in naïve CD8 T cells by targeting TMEM20.

Regulation of intracellular Ca signaling is a major determinant of CD8 T cell responsiveness, but the mechanisms underlying this regulation of Ca levels, especially in naïve CD8 T cells, are not fully defined. Here, we showed that microRNA-150 (miR-150) controls intracellular Ca levels in naïve CD8 T cells required for activation by suppressing TMEM20, a negative regulator of Ca extrusion. miR-150 deficiency increased TMEM20 expression, which resulted in increased intracellular Ca levels in naïve CD8 T cells.