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The role of IFN signaling in SARS-CoV-2 infection and outcome is still debated. Here, the authors longitudinally profiled plasma samples from hospitalized patients and show that a persistent inflammatory response is linked to delayed generation of adaptive immunity and increased risk of death when coupled with severe infection.

The mechanisms of pathological astrocyte responses during multiple sclerosis remain unclear. Kadowaki et al. found in MS mouse models that CLEC16A suppresses astrocyte pathogenic activities related to mitochondria by boosting mitophagy.

The first lasing results at SwissFEL, an X-ray free-electron laser, are presented, highlighting the facility’s unique capabilities. A general comparison to other major facilities is also provided.

Using animal models and clinical samples, the authors report that glioblastoma metabolites activate the transcription factor aryl hydrocarbon receptor in tumor-associated macrophages to modulate their function and T cell immunity, promoting tumor growth.

Since their initial operation, free-electron lasers are regularly upgraded in their performance and parameter control. Here the authors present the first lasing results of the soft X-ray free-electron laser beamline of the Paul Scherrer Institute, demonstrating different modes of operation and polarisation control of the tailored soft X-ray pulses.

Oligodendrocyte (OL) injury and loss is a pathologic hallmark of multiple sclerosis. Here, the authors show the presence of stress granules in OLs in multiple sclerosis lesions, and their in vitro studies in human OLs indicate that stress granules formation is a response to a combination of metabolic stress and pro-inflammatory conditions.

Endothelial cells release extracellular matrix components that regulate inflammation. Here the authors demonstrate that the extracellular matrix component epidermal growth factor-like protein 7 regulates inflammation in experimental autoimmune encephalomyelitis in the mouse.

Modulating the entry of inflammatory T cells into the brain could be one way to treat the autoimmune disease multiple sclerosis. Now, Frauke Zipp and colleagues demonstrate that activation of kinin receptor B1 can block autoimmune T cell migration into the brain and can therefore inhibit experimental autoimmune encephalomyelitis in mice.

In an experimental autoimmune encephalomyelitis model in mice, a subset of astrocytes retains an epigenetically regulated memory of past inflammation, causing exacerbated inflammation upon subsequent rechallenge.

Oxidized phosphatidylcholines found in MS lesions are not just markers of oxidative stress but are also promoters of demyelination and axon injury. Microglia suppress oxidized-phosphatidylcholine-mediated neurodegeneration by phagocytosis through TREM2.

Retinal pericytes connect via interpericyte tunnelling nanotubes into functional syncytia that regulate microcirculatory blood flow to help to match local blood flow with neuronal activity.

The pathogenic function of XBP1-expressing astrocytes in experimental autoimmune encephalomyelitis and multiple sclerosis have been studied using FIND-seq, a new method combining microfluidics cytometry, PCR-based detection of nucleic acids and cell sorting for in-depth single-cell transcriptomics analyses of rare cells.

Using single-cell and spatial transcriptomics, the authors identified several aging-associated and oxidized phosphatidylcholine-associated changes in microglia in the spinal cord, including an increase in osteopontin that contributed to neurodegeneration and neuroinflammation.

A subpopulation of astrocytes characterized by the expression of LAMP1 and TRAIL limits inflammation in the central nervous system through a mechanism involving the microbiota-modulated expression of IFNγ in meningeal natural killer cells.

Single-cell RNA sequencing of cells from humans with multiple sclerosis and mice with a model of the disease identifies a population of disease-promoting astrocytes in which anti-oxidant and anti-inflammatory proteins are suppressed.

A region on chromosome 19p13 is associated with the risk of developing ovarian and breast cancer. Here, the authors genotyped SNPs in this region in thousands of breast and ovarian cancer patients and identified SNPs associated with three genes, which were analysed with functional studies.

Cerebral malaria infection can provoke fatal neuroinflammation. Gros and colleagues identify an ubiquitin-modification axis that exacerbates neuroinflammation and that involves TRIM25 and USP15, which jointly promote type I interferon production.

After upregulation of AHR in astrocytes by type I interferons, commensal-microbe-derived metabolites of dietary tryptophan act on astrocytes to suppress CNS inflammation.

The authors use a combination of perceptual decision making in rats and computational modeling to explore the interplay of priors and sensory cues. They find that rats can learn to either alternate or repeat their actions based on reward likelihood and the influence of bias on their actions disappears after making an error.

In multiple sclerosis and experimental autoimmune encephalomyelitis, astrocytes produce lactosylceramide, a glycolipid that promotes astrocyte and microglial activation and immune cell infiltration into the CNS.

In this Review, Wiendl et al. consider how the study of rare but paradigmatic neuroimmunological diseases, including Susac syndrome, Rasmussen encephalitis and narcolepsy type 1, is providing fundamental insights into disease mechanisms that can be applied to more complex, heterogeneous neuroimmunological diseases such as multiple sclerosis.

Loss of miR-145 promotes remyelination in a chronically demyelinated animal model, implicating it as a factor in remyelination failure in human Multiple Sclerosis lesions and highlighting in as a potential therapeutic target for progressive MS.