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Here the authors show how the liver affects the immune response to pancreatic ductal adenocarcinoma and that cancer immunity and survival outcomes after surgery might be bolstered by therapeutic intervention on hepatocyte release of serum amyloid A proteins.
Roan et al. use Olink and single‐cell RNA sequencing (scRNA-seq) to show a dysregulated crosstalk between the cellular and humoral immune responses in individuals with long COVID 8 months postinfection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2).
Verdeil and colleagues show that the transcription factor NFAT5 is selectively required in tumor-induced, but not chronic infection-induced, CD8+ T cell exhaustion, possibly due to the modulation of NFAT5 activation by hyperosmolarity in the tumor environment.
To kill target cells, cytotoxic T lymphocytes (CTLs) form an immune synapse (IS) to elicit cell death and the IS then dissolves to allow for CTL serial killing. Huse et al. find that IS dissolution occurs concomitantly with cytoskeletal contraction of apoptotic targets and this is both necessary and sufficient for CTL dissociation
Immune cells are generally considered to be able to move through tissues using nonadhesive amoeboid migration mechanics. Here, the authors show that, unlike other immune cells, mast cells do not use this method and instead are completely reliant on integrin–ECM interactions.
The authors show that Nlrp10 can form a functional inflammasome in vitro and ex vivo, and that this inflammasome is protective in dextran sodium sulfate-induced colitis in mice.
NLRP10 has been considered as an inflammasome inhibitor. Here the authors show that upon mitochondrial rupture, NLRP10 assembles a canonical inflammasome and is highly expressed in differentiated keratinocytes, possibly supporting skin homeostasis.
Robbiani and colleagues show that antibodies against specific chemokines are detected in COVID-19 convalescents and may modulate the inflammatory response and disease outcome.
Maini and colleagues used bronchoalveolar lavage (BAL) samples from the lower respiratory tract of healthy donors obtained before the COVID-19 pandemic to show airway-resident cross-reactive T cells are present in pre-pandemic BAL, and correlated with the strength of human coronavirus immunity
Serafini and colleagues show that intestinal villus ILC3s, which are largely immotile at steady state, develop a patrolling behavior in response to inflammation.
Delaying a second COVID-19 vaccine dose is a common strategy to maximize vaccine coverage, but the immunological effects are unclear. Hall et al. demonstrate that a delayed second dose significantly enhances neutralizing humoral immunity.
Phetsouphanh and colleagues show that individuals with long COVID have persistent activation of the innate and adaptive immune system at 8 months after infection and define a set of analytes associated with long COVID.
The immunological processes occurring in the upper respiratory tract during COVID-19 are relatively poorly understood. Jochems and colleagues observe durable changes in the upper respiratory tract following SARS-CoV-2 infection, including evidence of virus-specific tissue memory T cells.
Lanz and colleagues show that the first dose of the BNT162b2 mRNA vaccine against SARS-CoV-2 activates a non-neutralizing recall response predominantly targeting the S2 subunit of the spike protein, while the second dose boosts neutralizing antibodies specific for the receptor binding domain of the spike protein.
ILC2 metabolism has been largely unexplored. Di Santo and colleagues examine metabolic profiles from naive and cytokine-activated ILC2s and find that IL-33-triggered ILC2s rely on distinct metabolic pathways to sustain proliferation and function.
Scheiermann and colleagues show that circadian clocks control the infiltration of dendritic cells into skin lymphatics in mice and humans, with a peak migration to the lymph nodes during the rest phase.
RIG-I is a cytosolic nucleic acid sensor triggering type I IFN production. Takaoka and colleagues find that RIG-I recognizes SARS-CoV-2 RNA in a noncanonical manner and fails to activate type I IFN, but it directly restricts viral replication.