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Pancreatic cancer has one of the worst survival outcomes of all cancers. Leinwand and Miller review the immunological landscape of pancreatic cancer, immune evasion mechanisms and the impact of the microbiota.
The combination of single-cell RNA-seq and in vivo CRISPR–Cas9 screens reveal a new circuit that directs germinal center B cells toward a memory B cell phenotype during viral infection.
Group 2 innate lymphoid cells (ILC2s) closely intersect with antitumor immunity. A new study describes how activation of lung-resident ILC2s orchestrates the suppression of natural killer cell–mediated innate antitumor immunity via an eosinophil-mediated metabolic mechanism.
Koliaraki, Prados, Armaka & Kollias review the roles of fibroblastic mesenchymal cells in tissue homeostasis and immunopathologic diseases, including chronic inflammatory disease, tissue fibrosis and cancer.
Durable responses to immunotherapy require the development of robust CD8+ T cell memory. A new study indicates that NRP1 differs from other checkpoint receptors as it functions as a checkpoint for the generation of memory.
A complex formed by the chemokine CXCL10 and commensal skin microbiota–derived DNA is a crucial component that triggers type I IFN responses to facilitate skin repair.
Guanylate-binding proteins (GBPs) promote immune defenses against infectious agents. Two studies reveal that GBP1 directly binds to cytosolic lipopolysaccharide (LPS), bringing caspase-4 to the surface of bacteria to induce pyroptosis.
In this Review, Smyth and colleagues provide an overview of recent advances in NK cell biology and discuss the progress and problems of NK cell–based cancer immunotherapies.
Antigen escape by solid tumors has limited the efficacy of genetically modified T cells. T cells engineered to secrete the cytokine Flt3L induce the activation of endogenous T cells, enabling a broader repertoire of tumor antigens to be targeted via the expansion of intratumoral antigen presenting cells, significantly improving tumor responses.
CAR T cells are engineered to recognize tumor-specific antigens and kill tumor cells. A study of CAR T cell activation using single-molecule microscopy reveals that CARs fail to efficiently convert antigen binding into early T cell signaling events.
Quantitative systems-level proteomics is cleverly used to reveal a dynamic program of protein turnover in naive and memory CD4+ T cells that, alongside a stockpile of metabolic protein machinery, poises the cells for activation.
Evolutionary genetic and experimental analyses suggest that mutations causing familial Mediterranean fever have been positively selected in the Middle East, probably because they confer heightened resistance against Yersinia pestis infection.
CXCR3+ regulatory T cells, known to limit type 1 immune responses, can promote tissue-resident immunity by providing bioactive transforming growth factor-β to CD8+ T cells.
Caspase-cleaved gasdermin D forms pores in cellular membranes, thus executing proinflammatory cell death by pyroptosis. Disulfiram — a drug used to treat chronic alcoholism — is now found to be an inhibitor of pore formation, which may therapeutically counteract exacerbated inflammation in sepsis and beyond.
The identification of the acute phase protein serum amyloid A as a soluble allergen sensor sheds new light on the mechanisms involved in the induction of type II airway inflammation.
A new report finds that peripheral immunization generates tissue-resident memory CD8+ T cells in the central nervous system that provide robust protection against local infection.
Host cell cholesterol is often exploited by pathogens for entry and egress. Two new studies elucidate a new interferon-inducible mechanism by which cells limit plasma membrane cholesterol to promote antibacterial defense.
B cells undergo iterative rounds of somatic hypermutation and selection for high-affinity antigen binding in the germinal center microenvironment. Two new studies provide insights into the temporal and spatial control mechanisms that act within B cells and follicular dendritic cells to jointly govern B cell differentiation and cell traffic within the GC.
A new study reports that TH2-coordinated tissue repair takes precedence over long-term protective immunity in urinary tract infections. Although effective in the interim, this can lead to recurrent infections and bladder dysfunction.
