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Here, the authors show that there is a pretumorigenic TH17 subset in the intestines that can convert to being tumorigenic under the control of KLF6 and that this process can be prevented by TGFβ1 production from intestinal epithelial cells.
Vinuesa et al. identify patients with systemic autoimmunity and a TNIP1 variant that result in dysregulated B cell function. Mice with the orthologous Tnip1 mutation develop spontaneous autoimmunity associated with impaired mitophagy and autophagic silencing of proteins downstream of Toll-like receptor 7 signaling.
Muppidi and colleagues show that loss of Gα13 drives B cell lymphomas preferentially in the mesenteric lymph nodes. They find that Gα13 is required to counteract mTORC1 and Myc signaling that is driven by the availability of dietary glutamine.
In this study, Uldrich and colleagues describe the crystal structure of the Vγ9Vδ2 T cell antigen receptor (TCR) interacting with BTN2A1 and demonstrate the existence of a second ligand that co-binds to a distinct epitope on Vγ9Vδ2 TCR. Using these data, the authors suggest a model of Vγ9Vδ2 TCR activation in which BTN2A1 and BTN3A1 are tethered to each other at the steady state, and must disengage to allow TCR binding.
Regulating the balance between TH17 cells that drive autoimmune inflammation and nonpathogenic TH17 cells is critical for limiting autoimmune pathology. Here, the authors extensively characterize these two cell states at the transcriptomic and epigenetic levels and show how BACH2 is protective in this context.
Seshadri, Davis and colleagues show that individuals who do not develop an infection with Mycobacterium tuberculosis (Mtb), despite exposure to the bacteria and expansion of CD4+ T cell clones specific to Mtb antigens, show enrichment of TH17 cell and T regulatory functional programs.
The thymus harbors a complex constitutively active inflammatory network with innate-like T cells representing one of its central nodes. Here, the authors show that these cells can induce tolerance to inflammation-associated self-antigens, a class of molecules that otherwise largely mirrors the spatial and temporal distribution of pathogen-derived antigens.
Qi and colleagues generate reporter mice that can track the stimulation history of individual B cells, a record epigenetically stored as progressive chromatin changes. This recording system revealed that the balance of B lymphocyte-induced maturation protein 1 (BLIMP1) to BTB domain and CNC homolog 2 (BACH2) predicts the fate of memory B cells upon recall challenge.
Lucas and colleagues show that differentiating B cells switch expression of PI3Kδ to PI3Kγ and that this switch is required for optimal T cell-dependent IgG antibody production in both mice and humans.
Single-cell technologies have unveiled a complex understanding of NK cells that has led to variations in nomenclature and inconsistencies across the scientific literature. Here, Vivier and colleagues used these technologies to dissect the heterogeneity of NK cells, revealing three prominent NK cell subsets in healthy human blood.
Malmberg and colleagues generated a single-cell transcriptional reference map to investigate pan-cancer profiles of tumor-infiltrating natural killer cells.
Dong and colleagues describe how TFH cells initially interact with dendritic cells in colonic lymphoid follicles and further differentiate into long-lived pathogenic TH1 cells, promoting the progression of colitis.
Humanized mice have been a valuable tool for modeling human immunology but are limited in their ability to model human antibody responses. Here the authors present their THX humanized mouse that does model human antibody responses and test its suitability for vaccination and autoimmunity studies.
Viiri and colleagues show that an orally administered transglutaminase 2 inhibitor prevented gluten-induced intestinal damage and inflammation at the transcriptional level.
SARS-CoV-2 has been shown to induce IL-1β-mediated neuroinflammation in humans and rodent models. Klein and colleagues show that low-dose COVID-19 vaccination prevents breakthrough infection-mediated hippocampal dysfunction and cognitive memory decline in mouse models.
Paiardini and colleagues describe a subset of lymph node HIV- and SIV-specific TOXhiTCF1+CD39+CD8+ T cells that coexhibit stem- and effector-like phenotypic and transcriptional profiles and associate with reduced viral burden.