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Our work identifies previously unrecognized functional heterogeneity in tissue-resident interstitial macrophages. We have identified ten macrophage subsets, each thought to specifically contribute to recruiting and organizing cell types within tissues. Moreover, our findings suggest the diversity and division of labor extend to other macrophage populations previously considered homogeneous.
In this Review, the authors analyze evidence for autoimmunity against components of antimicrobial immunity, metaphorically represented by the mythical ouroboros snake eating its own tail.
Homeostatic immune cells remain perpetually vigilant against pathogens. We found that baseline JAK–STAT signaling supports the characteristic transcriptional and epigenetic state of homeostatic T cells and macrophages in mice. JAK–STAT signaling under homeostatic conditions was driven by signals from healthy tissue and did not require external immune stimuli.
We report two patients with biallelic SHARPIN deficiency, which manifests with autoinflammation and B cell immunodeficiency and is phenotypically distinct from Sharpin deficiency in mice. In one patient, there was a significant shift from pro-survival signaling to cell-death signaling in fibroblasts and lymphoblasts induced by members of the TNF cytokine superfamily, accounting for the autoinflammation and immunodeficiency. Targeted therapy with TNF inhibitors had a dramatic beneficial effect.
The transient expression of CD61 and its unconventional pairing with CD103 at the immune synapse enhances T cell receptor signaling, improves anti-tumor cytotoxicity and mitigates tumor growth. Clinically, CD61+ tumor infiltrating lymphocytes (TILs) exhibit enhanced effector functions and show limited cellular exhaustion.
The microbiome is known to affect antitumor immune responses, but how this occurs is unclear. Rhamnose-rich polysaccharides (RHP) from a commensal strain of Lactiplantibacillus plantarum have now been shown to induce iron sequestration by tumor macrophages, thereby limiting tumor growth and promoting antitumor immunity.
The intestinal immune response is tightly controlled to limit inflammation, largely by the cytokine IL-10, which prevents colitis. We report that the transcription factors c-MAF and BLIMP-1 induced IL-10 in T cells in the colon, but also acted to negatively regulate distinct cytokine pathways to restrict pathobiont-induced colitis.
Age is the single greatest risk factor driving mortality after encounter with SARS-CoV-2. A new study shows that the composition of nasal epithelial cells varies across ages, facilitating SARS-CoV-2 growth and spread in older people.
Specialized T cell effector functions depend upon pre-established chromatin state. Cooperativity among PU.1, RUNX1 and BCL11B directs SWI–SNF complex recruitment to carry out chromatin priming at T cell effector loci during early thymic development.
MEF2C is a transcription factor that has known functions in a variety of cell types, but it has not yet been ascribed a role in natural killer cells. Data now show that MEF2C promotes the functional responses of human and murine natural killer cells by controlling their metabolic programs.
In this study, we use a transcriptomic approach as a starting point to explore the heterogeneity of human GATA3-expressing lymphocytes across different tissues and disease contexts. We identify, characterize and functionally validate an abundant progenitor-like memory T cell population with the potential to sustain pathogenic TH2 cell inflammation.
Profiling of plasma proteins in individuals with COVID-19 shows that complement activation and myeloid inflammation are major pathways in the pathogenesis of long COVID and identifies distinct profiles of immune dysregulation in individuals with long COVID, highlighting the heterogeneous and diverse nature of this disease.
In this Review, Kim et al. provide an overview of the prenatal immune conditions that contribute to the development of neurodevelopmental disorders and the immunological signatures and disorders associated with neurodevelopmental disorders.
Autoantibodies that develop in systemic lupus erythematosus (SLE) can cause long-term cognitive impairment that remains even after the systemic disease becomes quiescent. This study attributes the persistent cognitive symptoms of SLE to a self-sustaining neuroinflammatory process that continues indefinitely unless disrupted — which can be done using medications approved by the US Food and Drug Administration.
Understanding normal hematopoiesis is critical to understanding disease. Technological advances are driving insight into human hematopoiesis at unprecedented resolution. Integrating ‘-omics’ datasets with machine learning has yielded a high-resolution map of primary human bone marrow hematopoietic progenitor cells that supports the study of immune cell development, as well as the origins of disease.
DNA sensing for the purposes of innate immunity is tricky when the DNA sensor can easily become stuck on chromosomes during cell division. The mechanism by which the trapped DNA sensor is degraded — and how this process can be balanced with added immune protection — is now reported.
T cell- and antibody-based immunological protection are generally considered to function together, but data now show how T cells conferred by previous SARS-CoV-2 infection or two-dose vaccination can elicit heterologous protection in mice against subsequent SARS-CoV-2 infection, even in the absence of antibodies.
Granulosomes are novel complexes that feature an unexpected partnership between the tetraspanin CD63 and the inflammasome proteins NLRP3 and ASC. Granulosomes assemble on mast cell granules to propel them along microtubules to the plasma membrane for degranulation.
Drivers of persistent symptoms after acute COVID-19 remain largely unknown. Alterations in immune function, iron homeostasis and dysregulated erythropoiesis are described as treatable correlates of post-acute sequelae of COVID-19.