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After upregulation of AHR in astrocytes by type I interferons, commensal-microbe-derived metabolites of dietary tryptophan act on astrocytes to suppress CNS inflammation.
Fifty-five percent of individuals vaccinated with an attenuated Plasmodium falciparum sporozoite vaccine remained without parasitemia after controlled human malaria infection one year later; immune correlate analysis in humans and non-human primates suggest a role for liver-resident T cells.
Conditional expression of the most common somatic gain-of-function Ezh2 mutation in mouse models of melanoma and lymphoma reveals insight into its cooperation with other oncogenic events and its effects on the epigenome.
The cancer therapeutic cetuximab blocks EGFR signaling on tumor cells. Pozzi et al. now show that this antibody, when combined with chemotherapy, can also kill colorectal cancer cells by triggering immunogenic cell death.
Aberrant coupling between hippocampal interictal discharges and neocortical spindle oscillations triggers the generation of cortical ‘down’ states in both a rodent epilepsy model and human patients with focal epilepsy. In rats, this pathological network activity is shown to impair cognitive function.
Impaired TGF-β signaling due to SMAD4 mutation in PDAC tumors initiates a STAT3-dependent signaling cascade that leads to increased stromal stiffening and disease progression.
LGR4 has been identified as a new receptor for RANKL in bone cells where it opposes RANK signaling to inhibit osteoclasts differentiation, and its therapeutic targeting promotes reduced bone loss in three mouse models of osteoporosis.
Using proteomic analyses, Eric Rubin, Véronique Dartois and colleagues show that tuberculosis granulomas have spatially segregated protein compositions that compartmentalize pro- and anti-inflammatory responses to distinct regions.
The intestinal microbiota signals through epithelial cells to activate calcineurin and NFAT, driving proliferation of cancer stem cells and the development of colorectal cancer.
Grafting of caudalized rodent or human neural progenitor cells into sites of spinal cord injury enables true regeneration of damaged corticospinal axons in rodents. Regenerating axons form functional synapses within the graft, can extend beyond the lesion site, and help to support functional motor recovery.
ROR-γ antagonists suppress androgen receptor expression and growth of prostate tumors, but not of androgen-responsive healthy tissue, in preclinical models.
Alterations in the gut microbiota affect stroke outcomes via modulation of T cells, suggesting a gut-brain axis linking commensal microbes with the CNS.
Hessell et al. report that post-exposure treatment with HIV-1–specific neutralizing antibodies clears SHIV infection from the blood and tissues of infant rhesus macaques.
Analysis of SLOS patient-derived iPSCs reveals that cellular accumulation of the cholesterol precursor 7DHC, rather than cholesterol deficiency, causes dysregulation of Wnt/β-catenin signaling and aberrant neural differentiation.
In a rat model of spinal cord injury, calpain-dependent cleavage of motoneuron sodium channels can be pharmacologically targeted to achieve long-lasting amelioration of spasticity.
As beta cells age their levels of p16 rise, and the cells become senescent; rather than leading to dysfunction, this results in an increased capacity of the beta cells for glucose-stimulated insulin secretion.
Genomic analysis of a single metastasis informs about the oncogenic—and potentially druggable—genomic alterations present in other tumors within the same man with metastatic prostate cancer.