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m1A58 is a common tRNA modification that can influence protein translational efficiency. Here Liu et al. reveal that tRNA methylation controls in vivo T cell activation by enhancing translation of the key transcription factor Myc.
On 3–8 June 2022, the First International Aegean Conference on Mesenchymal Cells in Health & Disease took place in Chania, Crete, and brought together clinicians and scientists who work on mesenchymal or stromal cell biology across different fields including immunity, inflammation and cancer.
Immunotherapeutic targeting of the surface glycoprotein CD19 has markedly improved outcomes in patients with relapsed and refractory B cell progenitor acute lymphoblastic leukemia. Genome-wide CRISPR–Cas9 screening identifies modulators of CD19 mRNA processing that affect the abundance of the surface protein in human B cell leukemia cells, with the potential to improve antigen-directed immunotherapy efficacy.
During T cell activation, tRNA-m1A ‘writers’ TRMT61A and TRMT6 are upregulated to modify a group of early tRNA species and promote efficient translation of certain pre-cell-cycling proteins, thus ensuring rapid T cell proliferation and a timely adaptive immune response.
The explosion of single-cell and systems approaches in immunology risks leaving the uninitiated behind. This guide to systems immunology is designed for immunologists who want an introduction to the area.
Through access to healthy donors’ bronchoalveolar lavage (BAL) samples cryopreserved before the COVID-19 pandemic, we discovered CD4+ and CD8+ T cells able to cross-recognize SARS-CoV-2 among the airway tissue-resident memory pool. Pre-pandemic donors with detectable SARS-CoV-2-cross-reactive T cells in their airways also had stronger immunity to human seasonal coronaviruses.
A key biochemical event that enables T cells to discriminate between TCR antigens of varying affinities and to respond only to high-affinity antigens is full activation of the kinase ZAP70.
ETS1 regulates tissue-remodeling properties of specific fibroblast subtypes in the synovium, gut and cancer and thus emerges as a novel cross-tissue therapeutic target for modulation of pathogenic fibroblast activation.
The net effect of type I interferon (IFN-I) signaling on tumor control depends on various factors, including the potential engagement of adaptive anticancer immunity. New findings delineate a targetable epigenetic mechanism by which suboptimal IFN-I signaling promotes tumor progression in the context of cancer stem cell expansion and immunoevasion.
The role of eosinophils in response to cancer is not well understood. Here the authors document evidence that eosinophils contribute to the immune response to cancer and to immunotherapies and postulate that these cells might be more important than expected in these contexts.
Tissue-destructive fibroblasts in arthritis are driven by the transcription factor ETS1. Analysis of a cross-tissue, single-cell fibroblast dataset and genetic loss-of-function approaches further suggest that ETS1-expressing fibroblasts have a universal role in pathological tissue remodeling in multiple diseases, including arthritis, colitis and cancer.
The inhibitory checkpoint molecule CTLA-4 is essential for regulatory T cell function. A new study highlights the differential manner in which CTLA-4 binds CD80 and CD86, which determines its cellular fate and orchestrates immune tolerance regulation.
Wherry and colleagues describe how anti-PD-1 immunotherapy impacts outcomes of influenza vaccination in patients with cancer, and specifically, how it increases seroconversion and affects quantitative and qualitative aspects of antibodies and follicular T helper cell responses.
Multistep mechanosensing of lymphocyte infiltration and proliferation by the remodeling stroma and matrix underlies the immensely rapid and massive tissue expansion by lymph nodes in response to immune challenge.
Deacetylation of specific lysine residues in the DNA-binding domain of the transcription factors IRF3 and IRF7 by SIRT1 is necessary for liquid–liquid phase separation and transactivation of type I interferons. SIRT1 agonists partially restored the impaired innate immune responses in senescent cells and aged mice, suggestive of a possible strategy for preventing innate immunosenescence.
The response of circulating effector CD4 T cells to type I interferons (IFN-I) correlates with the overall survival of patients with cancer receiving immune checkpoint inhibition. IFN-I responsiveness is already epigenetically encoded before treatment initiation, highlighting a deterministic, clinically relevant feature that can predict therapeutic efficacy.
Boussiotis and colleagues review the hallmarks of tumor-associated macrophages and discuss the mechanisms that contribute to their pathophysiological adaptations to the tumor microenvironment.
Specific brain circuits recruited during stress contribute to differential immune responses and affect how the immune system handles viral and autoimmune challenges.
Immune checkpoint blocking therapies do not always work and come with some risks, but identifying non-responders and patients at risk of adverse events is becoming easier and more accurate.
