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Instructed by locally increased levels of glucocorticoids in the skin after acute hair loss, regulatory T cells communicate with hair follicle stem cells by producing TGFβ3 to stimulate stem-cell proliferation and hair regrowth.
Using high-resolution molecular and optical mapping of the three-dimensional genome, we found that the transcription factor TCF-1 is linked to changes in the structure of topologically associating domains in T cell progenitors that lead to interactions between previously insulated regulatory elements and target genes at late stages of T cell development.
Skin Treg cell crosstalk with hair-follicle stem cells (HFSCs) can control hair regrowth. Here the authors show that glucocorticoid receptor signaling in skin Treg cells induces TGF-β3, which in turn facilitates HFSC proliferation.
Social media has transformed the way we communicate science. Here is a step-by-step guide to promote the science of your own study or of others as a thread on Twitter.
Regulatory T cells that express high levels of IL-1R and ICOS display transcriptional features of antigen specificity, are highly suppressive and distinguish tumors from non-malignant inflamed tissues
Vahedi and colleagues show that TCF-1 promotes T cell development by minimizing the spatial distance between regulatory elements that are located within insulated neighborhoods in progenitor cells and are required for the expression of T cell genes.
Inflamed tissue has a special milieu, with hypoxia, high levels of metabolites from anaerobic glycolysis, and acidosis. Stimulation of a proton-activated receptor, TDAG8 (GPR65), in T cells has an important role in inflammatory bowel disease by balancing pro- and anti-inflammatory signals.
Extracellular microenvironments are more acidic upon tissue damage or in tumors. Xavier and colleagues identify a role for the pH-sensitive, G protein-coupled receptor GPR65 in multiple aspects of immune cell lipid metabolism, disruption of which leads to chronic inflammatory responses.
This study shows that systemic hypoxia alters the response of the bone marrow to inflammation by reducing type I interferon signaling and suppressing the accumulation of monocyte-derived macrophages in the lung. These events, in turn, hinder the resolution of lung inflammation.
Broadly protective antibodies to SARS-CoV-2 inform vaccine improvements and are directly used for treatment and prevention. New technologies are enabling the recovery of thousands of antibody examples, and workflows to rapidly identify the most potent examples are accelerating discovery.
A broadly neutralizing antibody (bnAb) response is required to combat SARS-CoV-2 variants of concern (VOCs). The authors isolated and characterized a large panel of sarbecovirus bnAbs from vaccinated individuals who had recovered from COVID-19, finding that many of these antibodies were able to neutralize all VOCs, including Omicron, and demonstrate prophylaxis in mice infected with diverse sarbecoviruses.
Breed et al. identify a subset of thymic SIRPα+ cDC2 dendritic cells that express CD301b, induced by type II cytokines, and high amounts of MHC-II. They find that the deletion of these cells can alter thymic CD4-single-positive repertoires, suggesting that they contribute to thymic tolerance.
Hypoxia alters populations of monocytes and macrophages during acute respiratory distress syndrome leading to persistent inflammation, a process that can be reversed by therapeutic administration of CSF1.
