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Quantitative mass spectrometry applied to T cell activation reveals key insights into signal-transduction pathways. These data identify selective alterations in the concentration of proteins in activated T cells and detail previously undescribed protein–protein interactions.
A new study has identified various previously unknown mutations in the genes encoding human and mouse A20 that affect its phosphorylation and its function as an inhibitor of the transcription factor NF-κB, with implications for immunity and inflammatory disease.
Zhu and colleagues discuss the forces that affect the ligand recognition, receptor triggering and signal transduction downstream of immunoreceptors, and their implication on lineage decision and effector function.
Cellular metabolic screening identifies hyper-respiration, induced by gain-of-function mutations in the gene encoding succinate dehydrogenase, as a disease-driving immunometabolic trait of B cells from patients with primary antibody deficiency.
A specifically engineered Zika subunit vaccine based on the viral envelope protein mediates protective immunity in mice without inducing the cross-reactive antibodies responsible for antibody-dependent enhancement of infection with dengue virus.
Transcription-factor paralogs are not equivalent and serve distinct roles in immune cells. Analysis of the RUNX family of transcription factors reveals insights into the non-redundant roles of RUNX1 and RUNX3.
Therapeutic efficacy in inflammatory diseases is hampered by disease complexity. A monoclonal antibody that neutralizes IL-1R3, the common co-receptor of most inflammatory IL-1 cytokines, opens up new perspectives in effective disease management.
The transcription factor TOX epigenetically reprograms CD8+ T cells to drive T cell exhaustion during chronic infection and cancer. Although they are necessary for T cell persistence, these changes contribute to diminished anti-tumor function in exhausted cells.
The NFIL3–ZEB2–ID2 transcription-factor regulatory circuit switches the E protein–dependent +41 kb Irf8 enhancer in DC progenitors to the BATF3-dependent +32 kb Irf8 enhancer in mature cDC1s. Deletion of the cryptic +41 kb Irf8 enhancer impedes cDC1 development.
GPD2, the mitochondrial glycerol-3-phosphate dehydrogenase, contributes to the shift in core metabolism in macrophages activated during infection and during the transition to an alternatively activated phenotype during tissue repair.
High-grade glioblastoma demonstrates exceedingly poor patient survival rates. In their Review, Lim and colleagues describe the immunological mechanisms involved in the control of glioblastoma and the outlook for immunotherapy.
Characterization of the self antigens that neonatal regulatory T cells recognize reveals dramatic effects of age and inflammation on the fate of T cells developing in the thymus.
Analysis of the whole-genome transcriptional activity of HIV-specific CD4+ T cells demonstrates distinct profiles associated with natural control of HIV replication, as well as dysfunctional phenotypes that persist even after effective antiretroviral therapy.
The American Course on Drug Development and Regulatory Science and the US National Institutes of Health held a workshop on cell-based immunotherapy on 22 January 2019.
A new report shows that upregulation of the receptor TREM1 on macrophages and neutrophils, dependent on the adrenergic nervous system, links stroke to systemic inflammation and gut barrier dysfunction, which result in bacterial translocation and exacerbation of neurological damage.
Epigenetic and transcriptional analyses of B cell subsets from patients with systemic lupus erythematosus reveal extensive effects of the disease environment and identify previously unknown connections and regulators of DN2 B cells and ABC-like cells.
Pierce and colleagues discuss the cellular consequences of BCR signaling and recent advances in the understanding of B cell signaling in context in vivo.
Underlying inflammatory bowel disease is a complex web of activated immune cells. In this Review, Neurath delineates the cells, pathways and signals that contribute to the pathology of inflammatory bowel disease and the potential for therapeutic intervention.
