Letters

Sun and colleagues report that the transcription factor TCF19 regulates calcium signaling and cell cycling progression in NK cells and is required for innate and adaptive NK cell responses to viral infection.

Mitochondrial electron transport chain activity provides ATP, generates superoxide, regulates apoptosis and provides the biosynthetic building blocks for growing cells. Here Steinert et al. genetically dissect these functions and find that, in the absence of mitochondrial complex III function, acute stimulation results in CD8⁺ T cell exhaustion and that mitochondrial complex III reactive oxygen species are required for establishment of naive and memory populations.

Sixt and colleagues show that, in environments where even the largest pores preclude free passage, leukocytes position their nucleus behind the centrosome and assemble a central F-actin pool that pushes outward to transiently dilate a path for the nucleus.

Bhattacharya and colleagues assess the impact of antigenic imprinting using samples from mRNA vaccinated or unvaccinated individuals primarily infected with the SARS-CoV-2 variants Delta and Omicron BA.1.

Panzer and colleagues show that the integrated stress response pathway regulates cytokine translation in CD4⁺ T_RM cells during homeostasis and inflammation.

Pyroptotic cell death results in inflammation. Here the authors find that F-actin-rich structures formed during macrophage pyroptosis persist after cell death to activate dendritic cells.

Liu and colleagues show that a previously described G396R variant of the human IGHG1 gene offers increased protection from SARS-CoV-2 and bacterial infections.

Appay and colleagues show that long-term antiretroviral therapy is associated with clonal succession of HIV-1-specific CD8⁺ T cell populations, which evolved from an exhaustion-like toward a stemness-like phenotype.

The transcriptional repressor Zbtb46 is expressed by DCs and endothelial cells. In this study, Choi and colleagues find downregulation of Zbtb46 confers a pro-tumor program in the vasculature and hematopoietic system, by promoting angiogenesis and the development of immunosuppressive myeloid cells.

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.

Openshaw and colleagues find myeloid inflammation and complement activation signatures in patients with long COVID who were previously hospitalized.

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

Huang and colleagues show that METTL3-mediated m⁶A mRNA modifications support the transcriptional activity of activated ILC2s.

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.

Aifantis and colleagues use leukemic cell lines to identify modulators of CD19 expression that have the potential to improve therapeutic strategies.