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.
Systemic lupus erythematosus (SLE) is an autoimmune disease with considerable clinical heterogeneity and diverse treatment options. A study now shows that heightened extrafollicular B cells and anti-BAFF therapy are linked to inferior responses to COVID-19 vaccines.
Here the authors dissect the contribution of IL-21 signaling to immune checkpoint-responding CD8+ T cells from mouse models and patients being treated for advanced melanoma.
Inflammasomes induce pyroptosis and, through poorly defined mechanisms, promote adaptive immune responses. High-resolution imaging of the explosive morphology of pyroptosis showed that minutes before rupture, gasdermin D instructs the cell to extend filopodia. These structures mark the corpses for recognition by the antigen-sampling receptor CLEC9A on dendritic cells.
Pyroptotic cell death results in inflammation. Here the authors find that F-actin-rich structures formed during macrophage pyroptosis persist after cell death to activate dendritic cells.
Tumor-antigen-specific CD8+ T cells are generally thought to help fight against cancer, but here the authors identify a subpopulation of CD8+ T cells that are associated with a poor clinical outcome in melanoma. Although these cells can recognize tumor antigens, they suppress cancer immunity.
Circulating immune stimuli access the joint through fenestrated capillaries that are located at the outer edge of the synovium. This area of vulnerability is policed by interacting macrophages and nociceptor neurons that work together as a functional unit.
In this Review, Sharma and colleagues describe the current landscape of combination therapies and discuss requirements for the development of effective combination strategies.
Why joints are highly responsive to systemic inflammation is unknown. Hasegawa et al. sought to address this question, developing a whole-mount imaging system of the entire synovium to profile the vascular, neuronal and immune components.
Here, the authors show that signal transducer and activator of transcription 3 (STAT3) has dual functions in small cell lung cancer as its deletion inhibited primary tumor growth but boosted metastatic spread. These seemingly opposing functions are a result of the requirement of STAT3 for stimulator of interferon genes–interferon signaling in metastasis and the authors show how it can be targeted in mice.
Ley and colleagues show that negative selection only partially explains the difference between CD4+ T cell responses to self and foreign peptides and that PD-1 and CD73 synergistically limit the CD4+ T cell responses to self.
In this Review, Herro and Grimes summarize the most recent key findings surrounding protective versus pathogenic functions of neutrophils, elaborating on phenotype-specific subsets of neutrophils and their involvement in homeostasis and disease.
Wang and colleagues show that in skeletal muscle cells and cardiomyocytes, the glucose transporter GLUT4 is a negative regulator of RIG-I-like receptor signaling during viral infection by redistributing RIG-I and MDA5 to the plasma membrane and attenuating interferon responses.
O’Shea and colleagues examine the three-dimensional chromatin architecture of the type 2 cytokine locus and how it differs between innate ILC2 cells and adaptive TH2 lymphocytes.
