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Robbiani and colleagues show that antibodies against specific chemokines are detected in COVID-19 convalescents and may modulate the inflammatory response and disease outcome.
Here, the authors show that CD8+ T cells egress from tumors via lymphatic vessels in a CXCL12/CXCR4-dependent manner. High-affinity antigen encounter inhibits CXCR4 and increases retention, while no encounter or weak affinity directs T cell exit to limit local tumor control.
Homozygous expression of MHC-II alleles that confer susceptibility to type 1 diabetes limits the efficiency of thymic negative selection and allows for CXCR6+ pathogenic clones to orchestrate the disease process. Expression of a second MHC-II allele decreases β-islet CD4+ T cell affinity, and limits CD8 cross-priming and diabetes risk without presenting the cognate MHC-II islet self-antigen.
A serendipitous behavioral observation in a mouse line led to the discovery that macrophages modulate acute pain. The macrophage-derived protein SNX25 sets the threshold for acute pain through tonic NGF signaling to cutaneous sensory neurons.
Unlike metabolic reprogramming that is characteristic of macrophage inflammatory polarization responses to lipopolysaccharide and TLR4 stimulation, the metabolism underlying inflammatory responses to CD40 signaling is not well characterized. Here the authors show CD40 signaling drives fatty acid oxidation and glutamine metabolism resulting in regulation of the NAD+/NADH ratio, which in turn promotes antitumor and pro-inflammatory macrophage functions.
The cholesterol metabolite receptor GPR183 regulates the secretion of IgA by intestinal plasma cells. This process requires epithelial cell sensing of commensal bacteria and the uptake of dietary cholesterol to generate the GPR183 ligand 7α,25-hydroxycholesterol. Upon GPR183 activation, IgA+ plasma cells remain at the center of intestinal villi and reduce their antibody secretion.
Type 1 diabetes is associated with homozygous expression of specific major histocompatibility complex class II beta chain polymorphisms. Here the authors show that the disease-protective effect of major histocompatibility complex class II heterozygosity is conferred by non-cognate thymocyte negative selection.
Benhar and colleagues provide an atlas of non-neuronal cells in the adult mouse retina at steady state and after optic nerve injury and identify key cellular and molecular events along the path of neuronal degeneration after injury.
Here, the authors show that acute influenza infection induces trained immunity in self-sustaining resident alveolar macrophages, which independently exert long-term antimetastatic immune surveillance in the lung via enhanced tumor killing.
Here the authors show that dihydroorotate dehydrogenase in the de novo pyrimidine synthesis pathway functions as a cell fate checkpoint that can be targeted to specifically diminish the number and function of effector T cells without affecting the memory T cell pool and response to infection.
