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The mechanism by which ingested material accesses the cytosol for cross-presentation is unclear. Caetano Reis e Sousa and colleagues demonstrate that signaling via the lectin receptor DNGR-1 ruptures the phagosome and releases its contents to the cytosol for cross-presentation.
Geisbert and colleagues report that African green monkeys infected with the SARS-CoV-2 virus develop disease symptoms that closely resemble those seen in infected humans, making this animal model a useful surrogate to investigate immune responses to coronavirus infection.
Stem cell–like memory (TSCM) CD8+ T cells are beneficial in antitumor responses, in part due to their ability to self-renew. Khleif and colleagues demonstrate that inhibition of the kinase MEK in CD8+ T cells favors induction of TSCM and superior antitumor responses.
Within a human cohort, wide variation can occur with constitutively expressed proteins. Aschenbrenner and colleagues found that individuals with lower CRELD1 expression have decreased frequencies of naive CD4+ T cells. Mice with conditional Creld1 deficiency also exhibit a phenotype associated with immunological aging.
COVID-19 is often characterized by a hyperinflammatory syndrome. Wang and colleagues show that low levels of IgG fucosylation enhance interactions with activating Fcγ receptors, boosting the inflammatory cytokines associated with severe COVID-19.
T cell memory formation is often described as occurring during the chronic phases of infection. Buchholz and colleagues use the phenomenon of ‘memory inflation’ following cytomegalovirus infection to show that a tiny subset of self-renewing T cells branch off early from the bulk population to generate memory.
Segal and colleagues identify a neuroprotective immature-like neutrophil subset that participates in dectin-1-dependent axon repair and regeneration in the central nervous system.
Exploring transcriptional heterogeneity of cKit+Sca1+ HSPCs using single cell RNA-sequencing, Naik and colleagues identify a population termed ‘lymphoid primed progenitors’ as the earliest stage of lymphoid lineage commitment, marked by downregulation of the stem/myeloid transcription factor Dach1.
The identity of stem-cell memory progenitor cells has been unclear. Lugli and colleagues use high-dimensional approaches to identify two new progenitor populations of human T cells—one giving rise to a functional lineage, the other to an exhausted-like one.
Sanz and colleagues examine B cell subsets in a cohort of patients with COVID-19. Severely ill patients have higher frequencies of activated extrafollicular T-bet+ B cells that form antibody-secreting cells, the majority of which express germline sequences and are reminiscent of antibody responses observed in patients with systemic lupus erythematosus during flares.
Sepsis is a biphasic disease characterized by an initial inflammatory phase, followed by a prolonged immunosuppression phase. Puthalakath and colleagues utilize a CRISPR-mediated mutagenesis screen to identify TREML4 as a regulator of sepsis-induced immunosuppression.
Humans with inherited defects in DOCK8 expression are prone to allergic, type 2 CD4+ T cell responses. Mandl and colleagues reveal an important role for cell death in driving such type 2 signals during infection.
Ho and colleagues report that mitochondrial dysfunction and impaired mitophagy triggered by the tumor microenvironment lead to subsequent epigenetic changes and cause permanent T cell exhaustion and dysfunction.
SARS-CoV-2-specific CD4+ and CD8+ T cell epitopes are found in both convalescent patients and virus-naive volunteers and are indicative of heterologous recognition shared with seasonal cold viruses.
The pathways controlling T follicular helper (TFH) cell development are only partially understood. Allen and colleagues demonstrate the importance of the T cell receptor, with low tonic signaling promoting TFH cell development and high tonic signaling opposing it.
Luster and colleagues show that Treg cells that reside in lung mucosa can respond to IL-33 upon allergen exposure and suppress innate cell responses. IL-33-activated ST2+ Treg cells secrete IL-35, which suppresses IL-17 production by γδ T cells and lessens eosinophil recruitment into the lung.
BATF3 is a member of the AP-1 transcription factor family. Kastenmüller and colleagues show that BATF3 is needed to promote memory CD8+ T cell responses. Activated CD8+ T cells transiently upregulate BATF3, which in turn suppresses expression of proapoptotic BIM to promote cell survival.
Phagocytes can acquire lipids and this modulates their function in a variety of disease states, such as atherosclerosis. Ren and colleagues demonstrate that neutrophils accumulate lipids and deliver them to tumor cells, which supports their proliferation, survival and metastasis.
Dysregulation of lung Treg cell function contributes to asthma development. Chatila and colleagues find that allergens upregulate Notch4–Hippo–Wnt signaling in Treg cells, triggering their release of GDF15 growth factor, which drives type 2 innate lymphoid cell activity and asthma.