Jessica L. McCord and al.

Analysis of a murine model of neonatal CMV infection reveals that blocking retinal T-cell infiltration, particularly through targeting the CXCR3 chemokine receptor, prevents the development of retinitis despite persistent infection.

Kristen E. Kay and al.

The anlysis of murine glioblastoma (GBM) models reveal an accumulation of spermidine, a polyamine, within the tumor microenvironment. Exogenous spermidine administration enhances tumor aggressiveness in an immunity-dependent manner by reducing the intratumoral density of CD8 T-cells and their cytotoxic functions. A Knockdown of the rate-limiting enzyme in spermidine synthesis does not affect GBM cell growth in vitro, confirming that the observed effect in vivo is mediated via the immune system.

Masaaki Okamoto and al.

In this study, the authors demonstrate that interferon-gamma (IFN-γ) polarizes regulatory T cells (Tregs) into T helper 1-like regulatory T cells (Th1-Tregs), which are essential for the histo-clinical remission of experimental autoimmune encephalomyelitis (EAE). Loss of IFN-γ signaling in Tregs and inhibition of T cell-derived IFN-γ disrupt Th1-Treg polarization and worsen the disease. Similarly, the selective ablation of Th1-Tregs promotes the pro-inflammatory functions of macrophages and exacerbates EAE.

Bin Wu and al.

The authors show that in mice, repeated exposure to threats leads to the priming of meningeal neutrophils, particularly in male individuals. Meningeal neutrophil activation correlates with a dampening of behavioral responses to threat signals. Knockout (KO) of the gene encoding CD177, a molecule associated with neutrophil activation, abolishes adaptation to repeated exposure to threats. Mechanistically, the authors demonstrate that CD177 promotes neutrophil polarization akin to that of Th1-type helper T cells. In turn, the neuronal signaling induced by these cytokines, particularly interferon-gamma (IFN-γ), enhances intrinsic GABAergic inhibition within the prelimbic cortex.

Fotios Koskeridis and al.

In this GWAS (genome-wide association study), the authors identified 16 loci associated with both Alzheimer’s disease and cardiovascular diseases. Two single nucleotide polymorphisms (SNPs) were prioritized: (i) rs11786896, which is associated with Alzheimer’s disease, atrial fibrillation, and the expression of the PLEC gene in the left cardiac ventricle; and (ii) rs7529220, which is associated with Alzheimer’s disease, atrial fibrillation, and the expression of genes from the C1q family. The authors demonstrate that under pathological conditions (Alzheimer’s disease or heart failure), the regulation of C1Q is driven by similar mechanisms in cardiac macrophages and microglial cells.