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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.
Obesity is often accompanied by chronic inflammation. Li and colleagues show that, in mice fed high-fat diets, IL-1 signaling in adipocytes induces an unconventional IRAK2 translocation to mitochondria and suppresses respiratory super-complex formation to alter mitochondrial function, and exacerbates obesity.
Autophagy controls cellular homeostasis and influences immune responses. Galluzzi and colleagues show that tumor cell autophagy opposes inflammatory cell death following radiation therapy and can be inhibited to enhance antitumor responses.
The CTLA-4–Ig fusion protein (abatacept) can have beneficial effects in autoimmune disease. Walker and colleagues show in mouse and human type 1 diabetes that abatacept targets pathogenic follicular helper T cells, and the frequencies of these cells at baseline can be used to stratify treatment responses in patients.
Pathological group 2 innate lymphoid cells (ILC2s) have mainly been implicated in allergy. Halim and colleagues demonstrate that ILC2s orchestrate a prometastatic pathway via the recruitment of eosinophils that suppress NK cell function.
Kim and colleagues provide new insights into the function and fate of neutrophils during influenza infection and their roles in antiviral T cell responses.
Verykokakis and colleagues show that the transcription factor BCL-6 is highly expressed in stage 0 NKT and is absolutely required for innate T cell lineage development. BCL-6 acts to modify the chromatin landscape and is needed to promote the ST0–ST1 transition and PLZF expression.
STING ER exit is the rate-limiting step in STING signaling, but the mechanism that drives this process is not understood. Paludan and colleagues identify CxORF56, called STEEP here, as a positive regulator of STING signaling.