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Yu et al. review the roles played by follicular helper T cells in sustaining germinal center B cell responses and vaccination strategies, as well as potential pathogenic autoimmune responses.
In airway epithelial cells, exposure to allergen proteases induces the stress granules-mediated transfer of IL-33 from the nucleus to the cytoplasm and extracellular release through gasdermin D pores containing a newly described active fragment.
Crystal structures of the immune checkpoint protein LAG3 reveal critical binding interfaces for inhibitory antibodies and cellular ligands, such as FGL1 and MHC class II molecules. These structures provide insight into the dimeric assembly of LAG3 proteins on the surface of T cells and suggest FGL1-induced clustering as an immunomodulatory mechanism.
A single-cell sequencing study shows that the human memory B cell repertoire is dominated by large IgM, IgG2 and IgA immunoglobulin families, whereas IgG1 families, including those specific for recall antigens, are of a small size. Multi-year analysis shows that memory B cell families are highly stable and that plasmablasts of T cell–independent and T cell–dependent isotypes are produced in a recurrent manner.
Extrathymic MHCII+Rorc+ Aire-expressing cells that share characteristics with type 3 innate lymphoid cells (ILC3s) internalize C. albicans and present its antigens, priming the development of Candida-specific TH17 cells.
Lymphocyte activation gene 3 (LAG3) is an important checkpoint inhibitor molecule of immunotherapeutic interest. New crystal structures of LAG3 provide important insight into its molecular architecture, laying the groundwork for future basic and applied investigations.
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.
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
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.
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.
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.
The dynamic changes in immune cell infiltration that accompany glioblastoma (GBM) progression remain obscure. Single-cell RNA sequencing and flow cytometry are now used to deconstruct the tumor immune microenvironment of early- and late-stage GBMs.
Intra-islet CD8+ T cells from a mouse model of type 1 diabetes exhibit an exhausted phenotype that differs from the canonical T cell exhaustion observed in cancer and chronic viral infection. Deletion of the inhibitory receptor LAG3 in these cells accelerated diabetes incidence and partially reversed this restrained phenotype.
Zehn and colleagues review the cellular fates and precursor trajectories that allow antigen-specific CD8+ T cells to persist in the face of chronic infection and cancer.
Inflammasomes function as immune-signaling platforms that assemble following pathogen detection. Direct binding of a viral protein to NLRP1 and the disruption of a previously unknown autoinhibitory NRLP1 complex drive the activation of the NLRP1 inflammasome independently of the proteasome.
Ectopic expression of IL-2 in the central nervous system (CNS) is sufficient to create an organ-restricted niche for tissue-resident regulatory T cells that support re-establishment of homeostasis after multiple types of tissue injury in the CNS.
