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Andreakos and colleagues provide a longitudinal study comparing patients with COVID-19 to patients infected with influenza. They report a dysregulated interferon response whereby IFN-λ and type I IFN production were diminished and delayed in patients with COVID-19, exhibiting a response that is ‘untuned’ with other inflammatory cytokines.
Mantovani and colleagues report elevated circulating concentrations of the long pentraxin PTX3 in patients with severe COVID-19. Within this cohort, early detection of high PTX3 concentrations emerged as a strong predictor of decreased survival.
Farber and colleagues report distinct antibody responses to SARS-CoV-2 in pediatric cohorts, including those who developed multisystem inflammatory syndrome (MIS-C), and adult COVID-19 cohorts.
Huppa and colleagues highlight signaling deficiencies in chimeric antigen receptor (CAR)-modified T cells that limit the efficacy of CAR T cell therapies to target tumors with diminished antigen expression.
van Loo and colleagues provide insights into the action of the anti-inflammatory protein A20. The ZnF7 and ZnF4 ubiquitin-binding domains of A20 are both required to suppress inflammatory signaling and cell death; however, these zinc fingers operate via distinct mechanisms.
Screaton and colleagues describe a protective Zika virus E-dimer-based subunit vaccine engineered to abrogate antibody-dependent enhancement of dengue infection.
NK cells recognize class I and stress-associated ligands. Altfeld and colleagues identify the NK cell receptor NKp44 as directly interacting with the class II HLA-DP in a partially peptide-dependent manner and with functional consequences for NK cell activity.
Dendritic cells (DCs) have been suggested to express a functional NLRP3 inflammasome. Gerlic and colleagues demonstrate, however, that bone marrow–derived DCs completely lack NLRP3 inflammasome activity and that the bulk of splenic DCs lack or have only minimal activity.
Yu and colleagues show that the transcription factor XBP1s positively regulates the cytolytic activity of human NK cells and is required for the IL-15-mediated survival of NK cells.
Harris and colleagues show that the cytokine TGF-β is required for colonization of the microglial niche and maintenance of central nervous system integrity. Acute loss of TGF-β leads to proinflammatory responses and fatal demyelinating disease.