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10.1186/s13073-021-00881-3

http://scihub22266oqcxt.onion/10.1186/s13073-021-00881-3
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33879239!8057009!33879239
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suck abstract from ncbi


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pmid33879239      Genome+Med 2021 ; 13 (1): 64
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  • IFN-gamma and TNF-alpha drive a CXCL10+ CCL2+ macrophage phenotype expanded in severe COVID-19 lungs and inflammatory diseases with tissue inflammation #MMPMID33879239
  • Zhang F; Mears JR; Shakib L; Beynor JI; Shanaj S; Korsunsky I; Nathan A; Donlin LT; Raychaudhuri S
  • Genome Med 2021[Apr]; 13 (1): 64 PMID33879239show ga
  • BACKGROUND: Immunosuppressive and anti-cytokine treatment may have a protective effect for patients with COVID-19. Understanding the immune cell states shared between COVID-19 and other inflammatory diseases with established therapies may help nominate immunomodulatory therapies. METHODS: To identify cellular phenotypes that may be shared across tissues affected by disparate inflammatory diseases, we developed a meta-analysis and integration pipeline that models and removes the effects of technology, tissue of origin, and donor that confound cell-type identification. Using this approach, we integrated > 300,000 single-cell transcriptomic profiles from COVID-19-affected lungs and tissues from healthy subjects and patients with five inflammatory diseases: rheumatoid arthritis (RA), Crohn's disease (CD), ulcerative colitis (UC), systemic lupus erythematosus (SLE), and interstitial lung disease. We tested the association of shared immune states with severe/inflamed status compared to healthy control using mixed-effects modeling. To define environmental factors within these tissues that shape shared macrophage phenotypes, we stimulated human blood-derived macrophages with defined combinations of inflammatory factors, emphasizing in particular antiviral interferons IFN-beta (IFN-beta) and IFN-gamma (IFN-gamma), and pro-inflammatory cytokines such as TNF. RESULTS: We built an immune cell reference consisting of > 300,000 single-cell profiles from 125 healthy or disease-affected donors from COVID-19 and five inflammatory diseases. We observed a CXCL10+ CCL2+ inflammatory macrophage state that is shared and strikingly abundant in severe COVID-19 bronchoalveolar lavage samples, inflamed RA synovium, inflamed CD ileum, and UC colon. These cells exhibited a distinct arrangement of pro-inflammatory and interferon response genes, including elevated levels of CXCL10, CXCL9, CCL2, CCL3, GBP1, STAT1, and IL1B. Further, we found this macrophage phenotype is induced upon co-stimulation by IFN-gamma and TNF-alpha. CONCLUSIONS: Our integrative analysis identified immune cell states shared across inflamed tissues affected by inflammatory diseases and COVID-19. Our study supports a key role for IFN-gamma together with TNF-alpha in driving an abundant inflammatory macrophage phenotype in severe COVID-19-affected lungs, as well as inflamed RA synovium, CD ileum, and UC colon, which may be targeted by existing immunomodulatory therapies.
  • |*SARS-CoV-2[MESH]
  • |Arthritis, Rheumatoid/genetics/immunology[MESH]
  • |Bronchoalveolar Lavage Fluid/cytology/immunology[MESH]
  • |COVID-19/genetics/*immunology[MESH]
  • |Colitis, Ulcerative/genetics/immunology[MESH]
  • |Colon/immunology[MESH]
  • |Crohn Disease/genetics/immunology[MESH]
  • |Cytokines/*immunology[MESH]
  • |Humans[MESH]
  • |Inflammation/genetics/immunology[MESH]
  • |Lung Diseases, Interstitial/genetics/immunology[MESH]
  • |Lung/immunology[MESH]
  • |Lupus Erythematosus, Systemic/genetics/immunology[MESH]
  • |Macrophages/*immunology[MESH]
  • |Phenotype[MESH]


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