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In part of a series of commissioned pieces on coronavirus disease 2019 (COVID-19), Sekaly and colleagues discuss COVID-19 vaccine progress, the underlying biology and prospects for the future.
Comparative analysis of SARS-CoV-2 isolates uncovers important mutations outside the spike gene that help the Alpha variant to operate under the radar of innate immune surveillance.
On 15–16 November 2021, the National Institute of Allergy and Infectious Diseases (NIAID), the National Cancer Institute (NCI) and the National Heart, Lung, and Blood Institute (NHLBI) hosted a virtual workshop on DEAD/DEAH-box RNA helicases in health and disease. The goal of the workshop was to review current advances, and identify knowledge gaps and future research to improve our understanding of the function of RNA helicases, and leverage these molecules as molecular targets with translational potential.
A delayed second dose relative to the standard 3-week schedule for the BNT162b2 mRNA vaccine against SARS-CoV-2 significantly raises the levels of neutralizing antibodies against SARS-CoV-2 variants.
The binding of PD-L1 to CD80 on antigen-presenting cells prevents PD-1 ligation on T cells. Therapeutic blockade of the cis-PD-L1–CD80 interaction liberates PD-L1 to bind to PD-1, inhibits autoreactive T cells and robustly alleviates autoimmune symptoms.
Crosstalk between the dendritic epidermal γδ T cell (DETC) T cell receptor and Skint1 expressed by keratinocytes at steady state regulates epidermal barrier function and maintains DETC responsiveness.
Immunogenic cell death (ICD) is central to both homeostatic and pathophysiological events. Kroemer et al. review the mechanisms of ICD and its role in therapy and disease.
LRRC8C is an essential component of volume-regulated anion channel (VRAC) in T cells. By mediating the transport of cGAMP, LRRC8C inhibits T cell function by activating STING and the tumor suppressor p53.
It is increasingly obvious that individuals are experiencing post-COVID-19 syndromes, or ‘long-haul COVID’. Here, Merad and Mehandru eview currently available knowledge of the underlying pathophysiological mechanisms of these sequelae, elaborating on persistent inflammation, induced autoimmunity and putative viral reservoirs.
Children are generally resistant to severe disease resulting from SARS-CoV-2 infection, but cases of pediatric COVID-19 and a new syndrome called MIS-C can occur. In this Review, the authors summarize what is known about the immunology of COVID-19 and MIS-C and how the pediatric response to SARS-CoV-2 is different from the immune response in adults.
A new study shows that the transcription factor KLF4 has a role in the maintenance of circadian immune responses. Loss of KLF4 activity contributes to the age-associated immune dysfunction.
Type 2 innate lymphoid cells (ILC2s) are implicated in lung diseases such as idiopathic pulmonary fibrosis, but targeting these cells is a challenge. New data show that neuropilin-1 drives the ILC2 phenotype and is specific to lung-resident ILC2s in mice.
Long-term persistence of memory CD4+ T cells is supported by mTORC2-dependent protection from a distinctive form of regulated cell death known as ferroptosis.
