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Concepcion et al. show that the volume-regulated anion channel LRRC8C mediates the transport of cGAMP in T cells, resulting in a noncanonical STING–p53-dependent suppression of Ca2+ influx, T cell proliferation and cytokine production.
It is increasingly obvious that individuals are experiencing post-COVID-19 syndromes, or ‘long-haul COVID’. Here, Merad and Mehandru eview currently available knowledge of the underlying pathophysiological mechanisms of these sequelae, elaborating on persistent inflammation, induced autoimmunity and putative viral reservoirs.
Children are generally resistant to severe disease resulting from SARS-CoV-2 infection, but cases of pediatric COVID-19 and a new syndrome called MIS-C can occur. In this Review, the authors summarize what is known about the immunology of COVID-19 and MIS-C and how the pediatric response to SARS-CoV-2 is different from the immune response in adults.
Becher and colleagues use a mouse model of multiple sclerosis to show that IFNγ is essential for the acquisition of a mature inflammatory phagocyte phenotype, while GM-CSF is required for phagocytosis and the production of IL-1β and ROS in Ly6Chi monocytes during neuroinflammation.
TNF is an important driver of many inflammatory diseases. Zhou et al. demonstrate ILC3 production of the growth factor HB-EGF protects against TNF-mediated injury of the gut epithelium in inflammatory bowel disease.
The function of type 3 innate lymphoid cells (ILC3s) in cancer is still poorly understood. Bruchard et al. demonstrate that ILC3s are critical for the recruitment of T cells to the tumor microenvironment and thereby play important roles in antitumor responses.
Stravalaci et al. examined recognition of SARS-CoV-2 by human soluble innate pattern recognition receptor. They report that pentraxin 3 and mannose-binding protein recognize viral nucleoprotein and spike, respectively. Mannose-binding lectin has antiviral activity, and human genetic polymorphisms of MBL2 are associated with more severe COVID-19.
Choe and colleagues show that intravital three-photon microscopy can be used to visualize the popliteal LN in mice and measure CD8+ T cells and CD4+ T cell motility through this paper shows T cell motility in the entire depthof T cell zone by ~635 um.
A new study shows that the transcription factor KLF4 has a role in the maintenance of circadian immune responses. Loss of KLF4 activity contributes to the age-associated immune dysfunction.
Type 2 innate lymphoid cells (ILC2s) are implicated in lung diseases such as idiopathic pulmonary fibrosis, but targeting these cells is a challenge. New data show that neuropilin-1 drives the ILC2 phenotype and is specific to lung-resident ILC2s in mice.
The consequences of climate change on human health are substantial and are now recognized as important contributors to allergic diseases. Thus, allergists and immunologists urgently need to take action to curtail its effect and modify its long-term course.
ILC2s are heterogeneous, dependent on tissue location. Here the authors show that TGFβ-induced neuropilin-1 specifically marks lung ILC2s and controls their function in pulmonary fibrosis by inducing expression of the ST2 IL-33 receptor.
Long-term persistence of memory CD4+ T cells is supported by mTORC2-dependent protection from a distinctive form of regulated cell death known as ferroptosis.
MIBI-TOF is a mass spectrometry-based multiplexed imaging platform that has been used to map tumors. In this Resource article, MIBI-TOF is used to provide a spatial atlas of immune responses within human tuberculosis granulomas.