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A genetic recorder of T cell replicative history identifies fewer accumulated divisions in a subset of CD8+ central memory T cells that shows stem-cell-like quiescence and superior recall capacity.
mRNA vaccines such as those used to prevent COVID-19 owe part of their success to methylation that masks immunostimulatory properties of the mRNA, but the immunological mechanisms of adjuvanticity are unclear. Two new studies reveal distinct mechanisms for innate sensing of this hidden adjuvant.
The formation of a provisional matrix is required for the onset of tissue repair. New research shows that neutrophils carry pre-existing matrix across organs into wounds, promoting fibroblast activation and scar formation.
B-cell-derived acetylcholine initiates a circuit that prompts bone marrow stromal cells to secrete factors that restrain the blood-forming activity of hematopoietic stem cells in response to cardiovascular dysfunction.
Targeting the post-translational modification enzyme QPCTL prevents the protection of CCL2 and CCL7 from N-terminal degradation, inactivates their chemotactic function and limits the recruitment of pro-tumoral macrophages.
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.
Zhong et al. exploit allelic variations in mice to pinpoint the ‘heavy lifter’ transcription factor families governing the chromatin landscape of resting and activated T cells.
New data show that, compared with adults, children infected by SARS-CoV-2 preferentially activate pre-existing immunity to endemic common-cold coronaviruses that are cross-reactive with SARS-CoV-2, with potential implications for pediatric vaccine strategies.
New research provides evidence of an impaired vitamin D gene signature in CD4+ T cells in patients with severe COVID-19. Mechanistically, it is shown that vitamin D alters the epigenetic landscape of CD4+ T cells, as well as inducing key transcription factors such as STAT3, BACH2 and JUN that reduce levels of IFN-γ and increase IL-10. These changes generate pro-resolving TH1 cells that may be beneficial in resolving or preventing severe COVID-19.
Chronic viral infections can trigger ineffective antibody responses. A new study shows that deletion of B cell-specific Moloney murine leukemia virus integration site 1 (BMI-1) from B cells restores protective antibodies during chronic infection.
In patients with rheumatoid arthritis, a short supply of aspartate in the mitochondria can force the endoplasmic reticulum of T cells to generate transmembrane TNF, which in turn contributes to synovial inflammation.
