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Treg cells are essential for immune homeostasis, but the transcription factors controlling their cellular identity are incompletely understood. Schumann and colleagues use pooled and arrayed CRISPR screens and scRNA-seq to describe key gene networks in human Treg cells.
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.
IL-17a is an evolutionarily conserved cytokine with behavior-modulating roles in the central nervous system. Kipnis and colleagues characterize a population of meningeal γδ17 T cells that use IL-17a to elicit anxiety-like behavior through cortical glutamatergic neurons.
The adhesion receptor CD2 plays an important role in the full activation of T cells. Dustin and colleagues show that CD2 occupies a region in the periphery of the immunological synapse where it amplifies cognate antigen signals, whereas the presence of PD-1 disrupts this effect.
Williams and colleagues investigate the origin, dynamics and transcriptional profiles of aortic intima macrophages during atherosclerosis disease progression.
Questions have arisen as to whether patients with severe COVID-19 disease can generate a T cell response against SARS-CoV-2. Tao Dong and colleagues report that convalescent patients with COVID-19 harbor functional memory CD4+ and CD8+ T cells that recognize multiple epitopes that span the viral proteome. CD4+ T cells predominated the memory response in patients with severe disease, whereas higher proportions of CD8+ T cells were found in patients with mild disease.
Antigen-activated B cells are short lived in the absence of a second signal provided by CD4+ T cells or cytokines. Zikherman and colleagues report that the NR4A family of nuclear receptors (NUR77 and NOR-1) are responsible for enforcing this ‘tolerance’ to self-antigen (signal 1 only) and explain, in part, why B cells are dependent upon a second signal.
B cell development and selection occur in the often hypoxic environment of the bone marrow. Burrows and colleagues demonstrate that dynamic regulation of B cell–intrinsic hypoxia-inducible factor-1α is essential for normal B cell development and function.
Checkpoint blockade is effective in only a subset of patients; therefore, biomarkers that can predict efficacy would be clinically highly valuable. Nishkawa and colleagues develop a biomarker based on PD-1 positivity of effector and regulatory T cells in the tumor microenvironment that accurately predicts the effectiveness of checkpoint blockade in patients.
NKG7 is a molecule well associated with NK cells but of unknown function. Engwerda and colleagues demonstrate that NKG7 is also associated with TH1 cells and is essential for type I and cytotoxic responses.
Takayanagi and colleagues show that thymic medullary fibroblasts can contribute to central tolerance mechanisms by expressing cell-type-specific antigens distinct from those expressed by medullary thymic epithelial cells.
Diamond and colleagues generate a K18-hACE2 model of SARS-CoV-2 infection that shares many features of severe COVID-19 infection and can be used to define the basis of lung disease and test immune and antiviral-based countermeasures.
The developmental timing for exhaustion is still obscure. Kallies and colleagues demonstrate that CD8+ T cell ‘exhaustion’ actually begins in the less-differentiated TCF1+ ‘precursor’ T cell pool during chronic viral infections.
The angiocrine Rspondin3 is produced by endothelial cells (ECs) and controls growth and development. Malik and colleagues show that lung ECs produce Rspondin3 following injury and specifically direct interstitial macrophages into an anti-inflammatory and wound-healing program.
Siracusa and colleagues reveal a regulatory role for basophils in the context of anti-helminth immunity and identify the neuropeptide neuromedin B as a potent inhibitor of type 2 inflammation.
Accurate serology testing is urgently needed to help diagnose SARS-CoV-2 infection. Here Valkenburg and colleagues use a luciferase immunoprecipitation system to assess the antibody responses to 15 different SARS-CoV-2 antigens in patients with COVID-19 and find ORF8 and ORF3b antibodies, taken together as a cluster of points, identified 96.5% of COVID-19 samples at early and late time points of disease with 99.5% specificity
Severe COVID-19 is characterized—among other things—by a hyperinflammatory state. Wang and colleagues describe the single-cell transcriptional landscape of moderate, severe and convalescent cases of patients with COVID-19.