Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain
the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in
Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles
and JavaScript.
RNA vaccines have been associated with high reactogenicity. Mellman and colleagues demonstrate that lipid-formulated RNA vaccines trigger IL-1 production and inflammation in humans but this pathway is dampened in mice.
Tumor-associated macrophages can restrict antitumor responses. Barreira da Silva and colleagues demonstrate that the intracellular enzyme QPCTL supports recruitment of immunomodulatory macrophages to the tumor microenvironment and its targeting can enhance tumor control.
Wragg and colleagues use MHC class II tetramers and TCRβ sequencing to track clonal populations of spike-specific CD4+ cTFH cells from cohorts of convalescent individuals with coronavirus disease 2019 or SARS-CoV-2-vaccinated individuals over 15 months.
How mRNA-based coronavirus disease 2019 vaccines drive immune responses is not clear. Here the authors characterize immune responses to the BNT162b2 vaccine in mice, and show how it stimulates innate immunity, with antigen-specific CD8+ T cell responses dependent on the RNA sensor MDA5.
Although COVID-19 vaccines are proving to be generally effective, new therapeutics to neutralize SARS-CoV-2 are required. Here, the authors engineer bispecific antibodies from ACE2-blocking B38 and H4 SARS-CoV-2 neutralizing antibodies and demonstrate their superiority in mice and nonhuman primates.
Raines et al. examine the role of the PERK-mediated ER stress response in promoting and sustaining M2-like macrophages in type 2 immune response and in tumor immunity.
Xue and colleagues show that the transcription factor Tcf1 preprograms a transcriptional program that supports the bioenergetic and proliferative needs of CD8+ central memory T cells in case of a secondary challenge.
Hayday and colleagues show that sustained Skint1-dependent interactions between murine intraepidermal γδ T cells and keratinocytes are required to maintain the homeostatic barrier function and phenotype of the intraepidermal γδ T cells, including their preparedness to respond appropriately to epidermal challenges.
Okazaki and colleagues develop and characterize monoclonal antibodies that co-opt T cell PD-1 activity. These antibodies can be used to ameliorate experimental autoimmune disease.
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.
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.
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.