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Recent decades have seen an alarming rise in the incidence of autoimmune disease. In a Perspective, Matarese and colleagues discuss the evidence showing that changes in diet and metabolic workload can account for, at least in part, rises in the frequency of autoimmune disease.
Gillet and colleagues find that infection with a gammaherpesvirus confers strong and lasting protection against airway allergy through the replacement of lung-resident alveolar macrophages with recruited regulatory monocytes of bone marrow origin.
Type 1 diabetes has a multifactorial etiology. Lehuen and colleagues demonstrate that MAIT cells serve both positive roles and negative roles in type 1 diabetes by maintaining gut integrity and limiting pancreatic inflammation but also directly destroying β-cells.
NLR proteins contribute to antiviral immune responses. Lemon and colleagues show that NLRX1 promotes antiviral responses in hepatocytes by competing with the kinase PKR for viral double-stranded RNA, which allows accumulation of the transcription factor IRF1 for early control of viral replication.
T cells developing in the thymus are signaled during positive selection to differentiate into either CD4+ T cells or CD8+ T cells. Singer and colleagues show that CD8+-lineage specification is signaled exclusively by cytokines, including cytokines that do not signal via the γc receptor, and that these are the only signals in the thymus that upregulate the transcription factor Runx3d to direct specification to the CD8+ lineage.
Diamond, Screaton and colleagues show that certain cross-reactive neutralizing antibodies to dengue virus have therapeutic activity against Zika virus infection in immune-privileged sites in vivo.
Cross-reactivity to dengue virus serotypes can trigger life-threatening inflammation. Culshaw et al. show that germline-encoded components of dengue-virus-specific TCRs influence antigen engagament and suggest that ‘innate-like’ recognition of the virus might underpin harmful cross-reactivity.
A two-amino-acid substitution in the transcription factor RORγt disrupts its effect in establishing the transcriptional program of TH17 cells while leaving its function in the development of thymocytes and lymphoid-tissue–inducer cells largely intact.
T-bet+NKp46+ subsets of group 1 and group 3 innate lymphoid cells within the meninges initiate neuroinflammation in central nervous system (CNS)-demyelinating disease by regulating both the stability of pathogenic T-bet+ T cells and their access to the CNS.