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The molecular basis for type I interferon (IFN)-mediated immunopathology is unclear. New data now identify the cGAS–STING pathway as a major driver of pathological type I IFN responses in COVID-19.
Increasingly, human monoclonal antibodies have been deployed against COVID-19, but combinations are typically needed for recognition of diverse viral variants. Bispecific antibodies could make the task of manufacturing and delivering combinations more efficient.
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.
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.
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.
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.