Neurological symptoms in SARS-CoV-2-infected patients have been reported, but their cause remains unclear. In theory, the neurological symptoms observed after SARS-CoV-2 infection could be (i) directly caused by the virus infecting brain cells, (ii) indirectly by our body’s local or systemic immune response towards the virus, (iii) by co-incidental phenomena or (iv) a combination of these factors.

The relevance of cross-dressing as an antigen presentation mechanism in antitumor responses is not fully understood. In this issue of Immunity, MacNabb et al. (2022) report that dendritic cells use cross-dressing as an effective mechanism to trigger CD8+ T cell antitumor immunity.

Distinct dendritic cell (DC) subsets exert specific functions in immune regulation, but their communication with each other has remained elusive. In this issue of Immunity, Gargaro et al. identify the IDO1-Kyn-AHR axis as a metabolic signaling pathway through which conventional DC subsets communicate and induce tolerogenicity.

Regulatory B cells infiltrate the microenvironment of solid tumors. However, their identification and characterization remain incomplete. In this issue of Immunity, Wang and colleagues characterize a new subset of leucine-induced regulatory B cells involved in colorectal cancer (CRC) immunoevasion in mice and humans.

In this issue of Immunity, Eisenstein, Hiliard, et al., uncover a novel mechanism of some widely used non-steroidal anti-inflammatory drugs (NSAIDs): activation of the antioxidant transcription factor NRF2 in myeloid immune cells.

The microbiome modulates brain function, but the precise routes of gut-brain communication remain unclear. In a recent issue of Science, Gabanyi et al. discover that hypothalamic GABAergic neurons directly recognize microbial muropeptides via NOD2, leading to reduced neuronal activity, loss of appetite, and aberrant thermoregulation.

Metastatic ovarian cancer is a significant clinical challenge due in part to its poor response to immunotherapy. In a recent issue of Cancer Cell, Anandon et al. (2022) identify a population of stem-like tissue-resident memory T cells that are responsible for the bulk of anti-tumor T cell immunity, with insights into improving therapeutic response.

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Abstract not available

Neutralizing antibodies can block infection, clear pathogens, and are essential to provide long-term immunity. Since the onset of the pandemic, SARS-CoV-2 neutralizing antibodies have been comprehensively investigated and critical information on their development, function, and potential use to prevent and treat COVID-19 have been revealed. With the emergence of SARS-CoV-2 immune escape variants, humoral

Identification of regulatory CD8+ T cells that suppress pathological immune responses is an importunate pursuit. In a recent issue of Science, Li et al. demonstrated that human KIR+CD8+ T cells suppress autoimmunity by eliminating pathogenic CD4+ T cells.

The brutal toll of another viral pandemic can be blunted by investing now in research that uncovers mechanisms of broad-based immunity so we may have vaccines and therapeutics at the ready. We do not know exactly what pathogen may trigger the next wave or next pandemic. We do know, however, that the human immune system must respond and must be bolstered with effective vaccines and other therapeutics

The lungs are constantly exposed to inhaled debris, allergens, pollutants, commensal or pathogenic microorganisms, and respiratory viruses. As a result, innate and adaptive immune responses in the respiratory tract are tightly regulated and are in continual flux between states of enhanced pathogen clearance, immune-modulation, and tissue repair. New single-cell-sequencing techniques are expanding our

Neuroanatomical barriers with physical, chemical, and immunological properties play an essential role in preventing the spread of peripheral infections into the CNS. A failure to contain pathogens within these barriers can result in very serious CNS diseases. CNS barriers are inhabited by an elaborate conglomerate of innate and adaptive immune cells that are highly responsive to environmental challenges

Pathogenic enteric viruses are a major cause of morbidity and mortality, particularly among children in developing countries. The host response to enteric viruses occurs primarily within the mucosa, where the intestinal immune system must balance protection against pathogens with tissue protection and tolerance to harmless commensal bacteria and food. Here, we summarize current knowledge in natural

In this issue of Immunity, Gideon et al. (2022) couple sophisticated single-cell analyses with detailed in vivo measurements of Mycobacterium tuberculosis granulomas to define the cellular and transcriptional properties of a successful host immune response during tuberculosis.

Although consistently implicated, the exact role of interferon (IFN) signaling in Alzheimer’s disease remains largely unexplored. Roy et al. now demonstrate that type I IFNs may drive cognitive dysfunction through acting not only on microglia but, surprisingly, also on neurons.

The mechanisms of how infectious diseases contribute to allergy remain unanswered. In this issue of Immunity, Agaronyan et al. (2022) show that Pseudomonas aeruginosa drives immune deviation through induction of type 2 immune responses, resulting in niche remodeling that incites allergic responses to innocuous antigens.

Many aspects of SARS-CoV-2 have fully conformed with the principles established by decades of viral immunology research, ultimately leading to the crowning achievement of highly effective COVID-19 vaccines. Nonetheless, the pandemic has also exposed areas where our fundamental knowledge is thinner. Some key unknowns are the duration of humoral immunity post-primary infection or vaccination and how

Macrophage colony stimulating factor-1 (CSF-1) plays a critical role in maintaining myeloid lineage cells. However, congenital global deficiency of CSF-1 (Csf1op/op) causes severe musculoskeletal defects that may indirectly affect hematopoiesis. Indeed, we show here that osteolineage-derived Csf1 prevented developmental abnormalities but had no effect on monopoiesis in adulthood. However, ubiquitous

Epithelial cells (tuft and goblet cells) interact with immune cells on the “inside” while secreting effector molecules into the topological “outside.” In this issue of Immunity, Zhao et al. investigate an interleukin-33 (IL-33) secretion mechanism in goblet cells dependent on O-GlcNAcylation and gasdermin pores facilitating worm expulsion.

Responsiveness to PD-1 blockade depends on a cell subset known as Tpex cells, but how these cells are sustained is less understood. In this issue of Immunity, Dähling et al. show how dendritic cells form a niche for Tpex preservation.

Interferon signaling mediates resistance to immune checkpoint blockade therapy, but the underlying mechanisms are poorly understood. In this issue of Immunity, Cucolo et al. identify RIPK1 as an interferon-stimulated gene with potent effects on cell extrinsic and intrinsic immunotherapy resistance.

Immune checkpoint blockade has dramatically improved cancer therapy but remains ineffective for most colorectal tumors. In this issue of Immunity, Peuker et al. describe a microbiota-myeloid-tumor cell crosstalk that inhibits CD8+ T cells and promotes colorectal cancer progression.

The impact of intestinal fungi on host physiology and their mechanisms of interaction are incompletely understood. In a recent issue of Cell, Leonardi et al. (2022) showed that mucosal fungi induce intestinal Th17 cells to produce IL-22 and IL-17A. IL-22 acts on the gut epithelium to protect barrier integrity, whereas IL-17 acts on IL-17RA+ neurons to enhance sociability.

The gut microbiome is well-known to shape local and distal immune responses, both in health and disease. In a recent issue of Nature, Hosang et al. demonstrate how the lung microbiome regulates the magnitude of autoimmune inflammation in the brain.

Nonresolving inflammation contributes to many diseases, including COVID-19 in its fatal and long forms. Our understanding of inflammation is rapidly evolving. Like the immune system of which it is a part, inflammation can now be seen as an interactive component of a homeostatic network with the endocrine and nervous systems. This review samples emerging insights regarding inflammatory memory, inflammatory