Monday, September 25, 2023
BestWooCommerceThemeBuilttoBoostSales-728x90

Innate immune memory in inflammatory arthritis – Nature Reviews Rheumatology


  • Vitetta, E. S. et al. Memory B and T cells. Annu. Rev. Immunol. 9, 193–217 (1991).

    Article 
    CAS 
    PubMed 

    Google Scholar
     

  • Netea, M. G., Quintin, J. & van der Meer, J. W. Trained immunity: a memory for innate host defense. Cell Host Microbe 9, 355–361 (2011).

    Article 
    CAS 
    PubMed 

    Google Scholar
     

  • Cerwenka, A. & Lanier, L. L. Natural killer cell memory in infection, inflammation and cancer. Nat. Rev. Immunol. 16, 112–123 (2016).

    Article 
    CAS 
    PubMed 

    Google Scholar
     

  • Netea, M. G. et al. Trained immunity: a program of innate immune memory in health and disease. Science 352, aaf1098 (2016).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Brandi, P. et al. Trained immunity induction by the inactivated mucosal vaccine MV130 protects against experimental viral respiratory infections. Cell Rep. 38, 110184 (2022).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Netea, M. G. et al. Trained immunity: a tool for reducing susceptibility to and the severity of SARS-CoV-2 infection. Cell 181, 969–977 (2020).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Kalafati, L. et al. Innate immune training of granulopoiesis promotes anti-tumor activity. Cell 183, 771–785.e712 (2020).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Geller, A. E. et al. The induction of peripheral trained immunity in the pancreas incites anti-tumor activity to control pancreatic cancer progression. Nat. Commun. 13, 759 (2022).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Bekkering, S. et al. Metabolic induction of trained immunity through the mevalonate pathway. Cell 172, 135–146.e139 (2018).

    Article 
    CAS 
    PubMed 

    Google Scholar
     

  • Goldblatt, F. & O’Neill, S. G. Clinical aspects of autoimmune rheumatic diseases. Lancet 382, 797–808 (2013).

    Article 
    CAS 
    PubMed 

    Google Scholar
     

  • Chaplin, D. D. Overview of the immune response. J. Allergy Clin. Immunol. 125, S3–S23 (2010).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Sakaguchi, S., Yamaguchi, T., Nomura, T. & Ono, M. Regulatory T cells and immune tolerance. Cell 133, 775–787 (2008).

    Article 
    CAS 
    PubMed 

    Google Scholar
     

  • Rawlings, D. J., Metzler, G., Wray-Dutra, M. & Jackson, S. W. Altered B cell signalling in autoimmunity. Nat. Rev. Immunol. 17, 421–436 (2017).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Maschmeyer, P. et al. Immunological memory in rheumatic inflammation — a roadblock to tolerance induction. Nat. Rev. Rheumatol. 17, 291–305 (2021).

    Article 
    CAS 
    PubMed 

    Google Scholar
     

  • Gerards, A. H. et al. Cyclosporin A monotherapy versus cyclosporin A and methotrexate combination therapy in patients with early rheumatoid arthritis: a double blind randomised placebo controlled trial. Ann. Rheum. Dis. 62, 291–296 (2003).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Yocum, D. E. et al. Safety of tacrolimus in patients with rheumatoid arthritis: long-term experience. Rheumatology 43, 992–999 (2004).

    Article 
    CAS 
    PubMed 

    Google Scholar
     

  • Mangoni, A. A. et al. Relapse rates after elective discontinuation of anti-TNF therapy in rheumatoid arthritis: a meta-analysis and review of literature. BMC Rheumatol. 3, 10 (2019).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Haschka, J. et al. Relapse rates in patients with rheumatoid arthritis in stable remission tapering or stopping antirheumatic therapy: interim results from the prospective randomised controlled RETRO study. Ann. Rheum. Dis. 75, 45–51 (2016).

    Article 
    PubMed 

    Google Scholar
     

  • Moore, J. et al. A pilot randomized trial comparing CD34-selected versus unmanipulated hemopoietic stem cell transplantation for severe, refractory rheumatoid arthritis. Arthritis Rheum. 46, 2301–2309 (2002).

    Article 
    CAS 
    PubMed 

    Google Scholar
     

  • Jaime-Pérez, J. C. et al. Autologous ATG-free hematopoietic stem cell transplantation for refractory autoimmune rheumatic diseases: a Latin American cohort. Clin. Rheumatol. 41, 869–876 (2022).

    Article 
    PubMed 

    Google Scholar
     

  • Teng, Y. K. et al. Long-term followup of health status in patients with severe rheumatoid arthritis after high-dose chemotherapy followed by autologous hematopoietic stem cell transplantation. Arthritis Rheum. 52, 2272–2276 (2005).

    Article 
    CAS 
    PubMed 

    Google Scholar
     

  • Mitroulis, I. et al. Modulation of myelopoiesis progenitors is an integral component of trained immunity. Cell 172, 147–161.e112 (2018).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Kaufmann, E. et al. BCG educates hematopoietic stem cells to generate protective innate immunity against tuberculosis. Cell 172, 176–190.e119 (2018).

    Article 
    CAS 
    PubMed 

    Google Scholar
     

  • Arts, R. J. W. et al. BCG vaccination protects against experimental viral infection in humans through the induction of cytokines associated with trained immunity. Cell Host Microbe 23, 89–100.e105 (2018).

    Article 
    CAS 
    PubMed 

    Google Scholar
     

  • Christ, A. et al. Western diet triggers NLRP3-dependent innate immune reprogramming. Cell 172, 162–175 e114 (2018).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Chavakis, T., Mitroulis, I. & Hajishengallis, G. Hematopoietic progenitor cells as integrative hubs for adaptation to and fine-tuning of inflammation. Nat. Immunol. 20, 802–811 (2019).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Theofilopoulos, A. N. et al. Sensors of the innate immune system: their link to rheumatic diseases. Nat. Rev. Rheumatol. 6, 146–156 (2010).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Murray, P. J. Macrophage polarization. Annu. Rev. Physiol. 79, 541–566 (2017).

    Article 
    CAS 
    PubMed 

    Google Scholar
     

  • Adamopoulos, I. E. et al. IL-17A gene transfer induces bone loss and epidermal hyperplasia associated with psoriatic arthritis. Ann. Rheum. Dis. 74, 1284–1292 (2015).

    Article 
    CAS 
    PubMed 

    Google Scholar
     

  • Adamopoulos, I. E. et al. IL-23 is critical for induction of arthritis, osteoclast formation, and maintenance of bone mass. J. Immunol. 187, 951–959 (2011).

    Article 
    CAS 
    PubMed 

    Google Scholar
     

  • Suzuki, E. et al. T cell-independent mechanisms associated with neutrophil extracellular trap formation and selective autophagy in IL-17A-mediated epidermal hyperplasia. J. Immunol. 197, 4403–4412 (2016).

    Article 
    CAS 
    PubMed 

    Google Scholar
     

  • Li, X. et al. Maladaptive innate immune training of myelopoiesis links inflammatory comorbidities. Cell 185, 1709–1727.e1718 (2022).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Stark, M. A. et al. Phagocytosis of apoptotic neutrophils regulates granulopoiesis via IL-23 and IL-17. Immunity 22, 285–294 (2005).

    Article 
    CAS 
    PubMed 

    Google Scholar
     

  • Mamedov, M. R. et al. A macrophage colony-stimulating-factor-producing γδ T cell subset prevents malarial parasitemic recurrence. Immunity 48, 350–363.e357 (2018).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Nguyen, C. T. et al. Peripheral γδ T cells regulate neutrophil expansion and recruitment in experimental psoriatic arthritis. Arthritis Rheumatol. 74, 1524–1534 (2022).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Venken, K. et al. RORγt inhibition selectively targets IL-17 producing iNKT and γδ-T cells enriched in spondyloarthritis patients. Nat. Commun. 10, 9 (2019).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Al-Mossawi, M. H. et al. Unique transcriptome signatures and GM-CSF expression in lymphocytes from patients with spondyloarthritis. Nat. Commun. 8, 1510 (2017).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Louis, C. et al. NK cell-derived GM-CSF potentiates inflammatory arthritis and is negatively regulated by CIS. J. Exp. Med. https://doi.org/10.1084/jem.20191421 (2020).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Oduro, K. A. Jr et al. Myeloid skewing in murine autoimmune arthritis occurs in hematopoietic stem and primitive progenitor cells. Blood 120, 2203–2213 (2012).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Chen, T. H., Swarnkar, G., Mbalaviele, G. & Abu-Amer, Y. Myeloid lineage skewing due to exacerbated NF-κB signaling facilitates osteopenia in Scurfy mice. Cell Death Dis. 6, e1723 (2015).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Haringman, J. J. et al. Synovial tissue macrophages: a sensitive biomarker for response to treatment in patients with rheumatoid arthritis. Ann. Rheum. Dis. 64, 834–838 (2005).

    Article 
    CAS 
    PubMed 

    Google Scholar
     

  • Soler Palacios, B. et al. Macrophages from the synovium of active rheumatoid arthritis exhibit an activin A-dependent pro-inflammatory profile. J. Pathol. 235, 515–526 (2015).

    Article 
    CAS 
    PubMed 

    Google Scholar
     

  • Katschke, K. J. Jr. et al. Differential expression of chemokine receptors on peripheral blood, synovial fluid, and synovial tissue monocytes/macrophages in rheumatoid arthritis. Arthritis Rheum. 44, 1022–1032 (2001).

    Article 
    CAS 
    PubMed 

    Google Scholar
     

  • Lacerte, P. et al. Overexpression of TLR2 and TLR9 on monocyte subsets of active rheumatoid arthritis patients contributes to enhance responsiveness to TLR agonists. Arthritis Res. Ther. 18, 10 (2016).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • van Kuijk, A. W., Reinders-Blankert, P., Smeets, T. J., Dijkmans, B. A. & Tak, P. P. Detailed analysis of the cell infiltrate and the expression of mediators of synovial inflammation and joint destruction in the synovium of patients with psoriatic arthritis: implications for treatment. Ann. Rheum. Dis. 65, 1551–1557 (2006).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Zhu, H. et al. CD16+ monocyte subset was enriched and functionally exacerbated in driving T-cell activation and B-cell response in systemic lupus erythematosus. Front. Immunol. 7, 512 (2016).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Hepburn, A. L., Mason, J. C. & Davies, K. A. Expression of Fcγ and complement receptors on peripheral blood monocytes in systemic lupus erythematosus and rheumatoid arthritis. Rheumatology 43, 547–554 (2004).

    Article 
    CAS 
    PubMed 

    Google Scholar
     

  • Katsiari, C. G. et al. Aberrant expression of the costimulatory molecule CD40 ligand on monocytes from patients with systemic lupus erythematosus. Clin. Immunol. 103, 54–62 (2002).

    Article 
    CAS 
    PubMed 

    Google Scholar
     

  • Mohammadi, S., Memarian, A., Sedighi, S., Behnampour, N. & Yazdani, Y. Immunoregulatory effects of indole-3-carbinol on monocyte-derived macrophages in systemic lupus erythematosus: a crucial role for aryl hydrocarbon receptor. Autoimmunity 51, 199–209 (2018).

    Article 
    CAS 
    PubMed 

    Google Scholar
     

  • Steinbach, F. et al. Monocytes from systemic lupus erythematous patients are severely altered in phenotype and lineage flexibility. Ann. Rheum. Dis. 59, 283–288 (2000).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Frostegård, J. et al. Lipid peroxidation is enhanced in patients with systemic lupus erythematosus and is associated with arterial and renal disease manifestations. Arthritis Rheum. 52, 192–200 (2005).

    Article 
    PubMed 

    Google Scholar
     

  • McGarry, T. et al. Rheumatoid arthritis CD14+ monocytes display metabolic and inflammatory dysfunction, a phenotype that precedes clinical manifestation of disease. Clin. Transl. Immunol. 10, e1237 (2021).

    Article 
    CAS 

    Google Scholar
     

  • Gordon, R. A., Grigoriev, G., Lee, A., Kalliolias, G. D. & Ivashkiv, L. B. The interferon signature and STAT1 expression in rheumatoid arthritis synovial fluid macrophages are induced by tumor necrosis factor α and counter-regulated by the synovial fluid microenvironment. Arthritis Rheum. 64, 3119–3128 (2012).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Hu, X. & Ivashkiv, L. B. Cross-regulation of signaling pathways by interferon-gamma: implications for immune responses and autoimmune diseases. Immunity 31, 539–550 (2009).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Qiao, Y. et al. Synergistic activation of inflammatory cytokine genes by interferon-γ-induced chromatin remodeling and toll-like receptor signaling. Immunity 39, 454–469 (2013).

    Article 
    CAS 
    PubMed 

    Google Scholar
     

  • Ivashkiv, L. B. IFNγ: signalling, epigenetics and roles in immunity, metabolism, disease and cancer immunotherapy. Nat. Rev. Immunol. 18, 545–558 (2018).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Fanucchi, S., Dominguez-Andres, J., Joosten, L. A. B., Netea, M. G. & Mhlanga, M. M. The intersection of epigenetics and metabolism in trained immunity. Immunity 54, 32–43 (2021).

    Article 
    CAS 
    PubMed 

    Google Scholar
     

  • Netea, M. G. et al. Defining trained immunity and its role in health and disease. Nat. Rev. Immunol. 20, 375–388 (2020).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Jha, A. K. et al. Network integration of parallel metabolic and transcriptional data reveals metabolic modules that regulate macrophage polarization. Immunity 42, 419–430 (2015).

    Article 
    CAS 
    PubMed 

    Google Scholar
     

  • Arts, R. J., Joosten, L. A. & Netea, M. G. Immunometabolic circuits in trained immunity. Semin. Immunol. 28, 425–430 (2016).

    Article 
    CAS 
    PubMed 

    Google Scholar
     

  • McNearney, T., Speegle, D., Lawand, N., Lisse, J. & Westlund, K. N. Excitatory amino acid profiles of synovial fluid from patients with arthritis. J. Rheumatol. 27, 739–745 (2000).

    CAS 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Kim, S. et al. Global metabolite profiling of synovial fluid for the specific diagnosis of rheumatoid arthritis from other inflammatory arthritis. PLoS One 9, e97501 (2014).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Rodgers, L. C. et al. The rheumatoid synovial environment alters fatty acid metabolism in human monocytes and enhances CCL20 secretion. Rheumatology 59, 869–878 (2020).

    Article 
    CAS 
    PubMed 

    Google Scholar
     

  • Meyer, A. et al. Syntenin-1-mediated arthritogenicity is advanced by reprogramming RA metabolic macrophages and Th1 cells. Ann. Rheum. Dis. https://doi.org/10.1136/ard-2022-223284 (2023).

    Article 
    PubMed 

    Google Scholar
     

  • Cheng, S. C. et al. mTOR- and HIF-1α-mediated aerobic glycolysis as metabolic basis for trained immunity. Science 345, 1250684 (2014).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Ballestar, E. & Li, T. New insights into the epigenetics of inflammatory rheumatic diseases. Nat. Rev. Rheumatol. 13, 593–605 (2017).

    Article 
    CAS 
    PubMed 

    Google Scholar
     

  • Zhang, Z. et al. H3K4 tri-methylation breadth at transcription start sites impacts the transcriptome of systemic lupus erythematosus. Clin. Epigenetics 8, 14 (2016).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Dai, Y., Zhang, L., Hu, C. & Zhang, Y. Genome-wide analysis of histone H3 lysine 4 trimethylation by ChIP-chip in peripheral blood mononuclear cells of systemic lupus erythematosus patients. Clin. Exp. Rheumatol. 28, 158–168 (2010).

    CAS 
    PubMed 

    Google Scholar
     

  • Wu, W. et al. Cystathionine-γ-lyase ameliorates the histone demethylase JMJD3-mediated autoimmune response in rheumatoid arthritis. Cell Mol. Immunol. 16, 694–705 (2019).

    Article 
    CAS 
    PubMed 

    Google Scholar
     

  • Mishra, N., Reilly, C. M., Brown, D. R., Ruiz, P. & Gilkeson, G. S. Histone deacetylase inhibitors modulate renal disease in the MRL-lpr/lpr mouse. J. Clin. Invest. 111, 539–552 (2003).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Zhao, Z. et al. Inhibition of histone H3 lysine-27 demethylase activity relieves rheumatoid arthritis symptoms via repression of IL6 transcription in macrophages. Front. Immunol. 13, 818070 (2022).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Lin, Y. C. et al. Tumor necrosis factor-α inhibitors suppress CCL2 chemokine in monocytes via epigenetic modification. Mol. Immunol. 83, 82–91 (2017).

    Article 
    CAS 
    PubMed 

    Google Scholar
     

  • Gebert, L. F. R. & MacRae, I. J. Regulation of microRNA function in animals. Nat. Rev. Mol. Cell Biol. 20, 21–37 (2019).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Seeley, J. J. et al. Induction of innate immune memory via microRNA targeting of chromatin remodelling factors. Nature 559, 114–119 (2018).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Kurowska-Stolarska, M. et al. MicroRNA-155 as a proinflammatory regulator in clinical and experimental arthritis. Proc. Natl Acad. Sci. USA 108, 11193–11198 (2011).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Yang, B. et al. Decreased miR-4512 levels in monocytes and macrophages of individuals with systemic lupus erythematosus contribute to innate immune activation and neutrophils NETosis by targeting TLR4 and CXCL2. Front. Immunol. 12, 756825 (2021).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Rodríguez-Ubreva, J. et al. Inflammatory cytokines shape a changing DNA methylome in monocytes mirroring disease activity in rheumatoid arthritis. Ann. Rheum. Dis. 78, 1505–1516 (2019).

    Article 
    PubMed 

    Google Scholar
     

  • de Andres, M. C. et al. Assessment of global DNA methylation in peripheral blood cell subpopulations of early rheumatoid arthritis before and after methotrexate. Arthritis Res. Ther. 17, 233 (2015).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Zhang, F. et al. Defining inflammatory cell states in rheumatoid arthritis joint synovial tissues by integrating single-cell transcriptomics and mass cytometry. Nat. Immunol. 20, 928–942 (2019).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Alivernini, S. et al. Distinct synovial tissue macrophage subsets regulate inflammation and remission in rheumatoid arthritis. Nat. Med. 26, 1295–1306 (2020).

    Article 
    CAS 
    PubMed 

    Google Scholar
     

  • Rothlin, C. V., Ghosh, S., Zuniga, E. I., Oldstone, M. B. & Lemke, G. TAM receptors are pleiotropic inhibitors of the innate immune response. Cell 131, 1124–1136 (2007).

    Article 
    CAS 
    PubMed 

    Google Scholar
     

  • Adomati, T. et al. Dead cells induce innate anergy via Mertk after acute viral infection. Cell Rep. 30, 3671–3681.e3675 (2020).

    Article 
    CAS 
    PubMed 

    Google Scholar
     

  • de Jong, H. M. Y. et al. Sustained remission with methotrexate monotherapy after 22-week induction treatment with TNF-α inhibitor and methotrexate in early psoriatic arthritis: an open-label extension of a randomized placebo-controlled trial. Arthritis Res. Ther. 21, 208 (2019).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Degboé, Y. et al. Polarization of rheumatoid macrophages by TNF targeting through an IL-10/STAT3 mechanism. Front. Immunol. 10, 3 (2019).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Municio, C. et al. Methotrexate limits inflammation through an A20-dependent cross-tolerance mechanism. Ann. Rheum. Dis. 77, 752–759 (2018).

    Article 
    CAS 
    PubMed 

    Google Scholar
     

  • Xia, M. et al. Histone methyltransferase Ash1l suppresses interleukin-6 production and inflammatory autoimmune diseases by inducing the ubiquitin-editing enzyme A20. Immunity 39, 470–481 (2013).

    Article 
    CAS 
    PubMed 

    Google Scholar
     

  • Tsukasaki, M. & Takayanagi, H. Osteoimmunology: evolving concepts in bone-immune interactions in health and disease. Nat. Rev. Immunol. 19, 626–642 (2019).

    Article 
    CAS 
    PubMed 

    Google Scholar
     

  • Teitelbaum, S. L. & Ross, F. P. Genetic regulation of osteoclast development and function. Nat. Rev. Genet. 4, 638–649 (2003).

    Article 
    CAS 
    PubMed 

    Google Scholar
     

  • Fierro, F. A., Nolta, J. A. & Adamopoulos, I. E. Concise review: stem cells in osteoimmunology. Stem Cell 35, 1461–1467 (2017).

    Article 

    Google Scholar
     

  • Adamopoulos, I. E. et al. Synovial fluid macrophages are capable of osteoclast formation and resorption. J. Pathol. 208, 35–43 (2006).

    Article 
    CAS 
    PubMed 

    Google Scholar
     

  • Adamopoulos, I. E. & Mellins, E. D. Alternative pathways of osteoclastogenesis in inflammatory arthritis. Nat. Rev. Rheumatol. 11, 189–194 (2015).

    Article 
    CAS 
    PubMed 

    Google Scholar
     

  • Adamopoulos, I. E. et al. Interleukin-17A upregulates receptor activator of NF-κB on osteoclast precursors. Arthritis Res. Ther. 12, R29 (2010).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Shin, H. S. et al. Crosstalk among IL-23 and DNAX activating protein of 12 kDa-dependent pathways promotes osteoclastogenesis. J. Immunol. 194, 316–324 (2015).

    Article 
    CAS 
    PubMed 

    Google Scholar
     

  • Yarilina, A., Xu, K., Chen, J. & Ivashkiv, L. B. TNF activates calcium-nuclear factor of activated T cells (NFAT)c1 signaling pathways in human macrophages. Proc. Natl Acad. Sci. USA 108, 1573–1578 (2011).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Furuya, H. et al. Interleukin-23 regulates inflammatory osteoclastogenesis via activation of CLEC5A+ osteoclast precursors. Arthritis Rheumatol. https://doi.org/10.1002/art.42478 (2023).

    Article 
    PubMed 

    Google Scholar
     

  • Andreev, D. et al. Osteocyte necrosis triggers osteoclast-mediated bone loss through macrophage-inducible C-type lectin. J. Clin. Invest. 130, 4811–4830 (2020).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Nishikawa, K. et al. DNA methyltransferase 3a regulates osteoclast differentiation by coupling to an S-adenosylmethionine-producing metabolic pathway. Nat. Med. 21, 281–287 (2015).

    Article 
    CAS 
    PubMed 

    Google Scholar
     

  • Indo, Y. et al. Metabolic regulation of osteoclast differentiation and function. J. Bone Miner. Res. 28, 2392–2399 (2013).

    Article 
    CAS 
    PubMed 

    Google Scholar
     

  • Murata, K. et al. Hypoxia-sensitive COMMD1 integrates signaling and cellular metabolism in human macrophages and suppresses osteoclastogenesis. Immunity 47, 66–79.e65 (2017).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Kim, K., Shin, Y., Kim, J., Ulmer, T. S. & An, W. H3K27me1 is essential for MMP-9-dependent H3N-terminal tail proteolysis during osteoclastogenesis. Epigenetics Chromatin 11, 23 (2018).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Xia, Y. et al. TGFβ reprograms TNF stimulation of macrophages towards a non-canonical pathway driving inflammatory osteoclastogenesis. Nat. Commun. 13, 3920 (2022).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Kurotaki, D., Yoshida, H. & Tamura, T. Epigenetic and transcriptional regulation of osteoclast differentiation. Bone 138, 115471 (2020).

    Article 
    CAS 
    PubMed 

    Google Scholar
     

  • Kameda, Y. et al. Siglec-15 regulates osteoclast differentiation by modulating RANKL-induced phosphatidylinositol 3-kinase/Akt and Erk pathways in association with signaling Adaptor DAP12. J. Bone Miner. Res. 28, 2463–2475 (2013).

    Article 
    CAS 
    PubMed 

    Google Scholar
     

  • Moorlag, S. et al. An integrative genomics approach identifies KDM4 as a modulator of trained immunity. Eur. J. Immunol. 52, 431–446 (2022).

    Article 
    CAS 
    PubMed 

    Google Scholar
     

  • McDonald, M. M. et al. Osteoclasts recycle via osteomorphs during RANKL-stimulated bone resorption. Cell 184, 1940 (2021).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Tsourdi, E. et al. Discontinuation of denosumab therapy for osteoporosis: a systematic review and position statement by ECTS. Bone 105, 11–17 (2017).

    Article 
    PubMed 

    Google Scholar
     

  • Kiesel, J. R., Buchwald, Z. S. & Aurora, R. Cross-presentation by osteoclasts induces FoxP3 in CD8+ T cells. J. Immunol. 182, 5477–5487 (2009).

    Article 
    CAS 
    PubMed 

    Google Scholar
     

  • Li, H. et al. Cross talk between the bone and immune systems: osteoclasts function as antigen-presenting cells and activate CD4+ and CD8+ T cells. Blood 116, 210–217 (2010).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Ibáñez, L. et al. Inflammatory osteoclasts prime TNFα-producing CD4+ T cells and express CX3 CR1. J. Bone Miner. Res. 31, 1899–1908 (2016).

    Article 
    PubMed 

    Google Scholar
     

  • Madel, M. B. et al. Dissecting the phenotypic and functional heterogeneity of mouse inflammatory osteoclasts by the expression of Cx3cr1. Elife https://doi.org/10.7554/eLife.54493 (2020).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Prevoo, M. L. et al. Remission in a prospective study of patients with rheumatoid arthritis. American Rheumatism Association preliminary remission criteria in relation to the disease activity score. Br. J. Rheumatol. 35, 1101–1105 (1996).

    Article 
    CAS 
    PubMed 

    Google Scholar
     

  • Alivernini, S. et al. Synovial features of patients with rheumatoid arthritis and psoriatic arthritis in clinical and ultrasound remission differ under anti-TNF therapy: a clue to interpret different chances of relapse after clinical remission? Ann. Rheum. Dis. 76, 1228–1236 (2017).

    Article 
    CAS 
    PubMed 

    Google Scholar
     

  • Tokai, N. et al. Predictive value of bone destruction and duration of clinical remission for subclinical synovitis in rheumatoid arthritis patients. Mod. Rheumatol. 25, 540–545 (2015).

    Article 
    PubMed 

    Google Scholar
     

  • Knowlton, N. et al. The meaning of clinical remission in polyarticular juvenile idiopathic arthritis: gene expression profiling in peripheral blood mononuclear cells identifies distinct disease states. Arthritis Rheum. 60, 892–900 (2009).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Misharin, A. V. et al. Nonclassical Ly6C monocytes drive the development of inflammatory arthritis in mice. Cell Rep. 9, 591–604 (2014).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • van Nies, J. A. et al. What is the evidence for the presence of a therapeutic window of opportunity in rheumatoid arthritis? A systematic literature review. Ann. Rheum. Dis. 73, 861–870 (2014).

    Article 
    PubMed 

    Google Scholar
     

  • van Mens, L. J. J. et al. Achieving remission in psoriatic arthritis by early initiation of TNF inhibition: a double-blind, randomised, placebo-controlled trial of golimumab plus methotrexate versus placebo plus methotrexate. Ann. Rheum. Dis. 78, 610–616 (2019).

    Article 
    PubMed 

    Google Scholar
     

  • Krijbolder, D. I. et al. Intervention with methotrexate in patients with arthralgia at risk of rheumatoid arthritis to reduce the development of persistent arthritis and its disease burden (TREAT EARLIER): a randomised, double-blind, placebo-controlled, proof-of-concept trial. Lancet 400, 283–294 (2022).

    Article 
    PubMed 

    Google Scholar
     

  • Aeberli, D. et al. Regulation of peripheral classical and non-classical monocytes on infliximab treatment in patients with rheumatoid arthritis and ankylosing spondylitis. RMD Open 2, e000079 (2016).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Vos, A. C. et al. Anti-tumor necrosis factor-α antibodies induce regulatory macrophages in an Fc region-dependent manner. Gastroenterology 140, 221–230 (2011).

    Article 
    CAS 
    PubMed 

    Google Scholar
     

  • Saleem, B. et al. Can flare be predicted in DMARD treated RA patients in remission, and is it important? A cohort study. Ann. Rheum. Dis. 71, 1316–1321 (2012).

    Article 
    PubMed 

    Google Scholar
     

  • Chen, H. H. et al. Association between a history of periodontitis and the risk of rheumatoid arthritis: a nationwide, population-based, case-control study. Ann. Rheum. Dis. 72, 1206–1211 (2013).

    Article 
    PubMed 

    Google Scholar
     

  • Mikuls, T. R. et al. Porphyromonas gingivalis and disease-related autoantibodies in individuals at increased risk of rheumatoid arthritis. Arthritis Rheum. 64, 3522–3530 (2012).

    Article 
    CAS 
    PubMed 

    Google Scholar
     

  • Sandberg, M. E., Bengtsson, C., Klareskog, L., Alfredsson, L. & Saevarsdottir, S. Recent infections are associated with decreased risk of rheumatoid arthritis: a population-based case-control study. Ann. Rheum. Dis. 74, 904–907 (2015).

    Article 
    PubMed 

    Google Scholar
     

  • Biswas, S. K. & Lopez-Collazo, E. Endotoxin tolerance: new mechanisms, molecules and clinical significance. Trends Immunol. 30, 475–487 (2009).

    Article 
    CAS 
    PubMed 

    Google Scholar
     

  • Jeljeli, M. et al. Macrophage immune memory controls endometriosis in mice and humans. Cell Rep. 33, 108325 (2020).

    Article 
    CAS 
    PubMed 

    Google Scholar
     

  • Bekkering, S. et al. Oxidized low-density lipoprotein induces long-term proinflammatory cytokine production and foam cell formation via epigenetic reprogramming of monocytes. Arterioscler. Thromb. Vasc. Biol. 34, 1731–1738 (2014).

    Article 
    CAS 
    PubMed 

    Google Scholar
     

  • Geng, S. et al. The persistence of low-grade inflammatory monocytes contributes to aggravated atherosclerosis. Nat. Commun. 7, 13436 (2016).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Fuentelsaz-Romero, S. et al. The macrophage reprogramming ability of antifolates reveals soluble CD14 as a potential biomarker for methotrexate response in rheumatoid arthritis. Front. Immunol. 12, 776879 (2021).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Vaugelade, J., Pinchinat, S., Guiella, G., Elguero, E. & Simondon, F. Non-specific effects of vaccination on child survival: prospective cohort study in Burkina Faso. Br. Med. J. 329, 1309 (2004).

    Article 
    CAS 

    Google Scholar
     

  • Kleinnijenhuis, J. et al. Bacille Calmette-Guerin induces NOD2-dependent nonspecific protection from reinfection via epigenetic reprogramming of monocytes. Proc. Natl Acad. Sci. USA 109, 17537–17542 (2012).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Quintin, J. et al. Candida albicans infection affords protection against reinfection via functional reprogramming of monocytes. Cell Host Microbe 12, 223–232 (2012).

    Article 
    CAS 
    PubMed 

    Google Scholar
     

  • Jeljeli, M. et al. Trained immunity modulates inflammation-induced fibrosis. Nat. Commun. 10, 5670 (2019).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Saz-Leal, P. et al. Targeting SHIP-1 in myeloid cells enhances trained immunity and boosts response to infection. Cell Rep. 25, 1118–1126 (2018).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Foster, S. L., Hargreaves, D. C. & Medzhitov, R. Gene-specific control of inflammation by TLR-induced chromatin modifications. Nature 447, 972–978 (2007).

    Article 
    CAS 
    PubMed 

    Google Scholar
     

  • Cunningham, K. T., Finlay, C. M. & Mills, K. H. G. Helminth imprinting of hematopoietic stem cells sustains anti-inflammatory trained innate immunity that attenuates autoimmune disease. J. Immunol. 206, 1618–1630 (2021).

    Article 
    CAS 
    PubMed 

    Google Scholar
     

  • Martinez-Gonzalez, I. et al. Allergen-experienced group 2 innate lymphoid cells acquire memory-like properties and enhance allergic lung inflammation. Immunity 45, 198–208 (2016).

    Article 
    CAS 
    PubMed 

    Google Scholar
     

  • Ardain, A. et al. Group 3 innate lymphoid cells mediate early protective immunity against tuberculosis. Nature 570, 528–532 (2019).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Naik, S. et al. Inflammatory memory sensitizes skin epithelial stem cells to tissue damage. Nature 550, 475–480 (2017).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Hamada, A., Torre, C., Drancourt, M. & Ghigo, E. Trained immunity carried by non-immune cells. Front. Microbiol. https://doi.org/10.3389/fmicb.2018.03225 (2019).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Arts, R. J. et al. Glutaminolysis and fumarate accumulation integrate immunometabolic and epigenetic programs in trained immunity. Cell Metab. 24, 807–819 (2016).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Jentho, E. et al. Trained innate immunity, long-lasting epigenetic modulation, and skewed myelopoiesis by heme. Proc. Natl Acad. Sci. USA https://doi.org/10.1073/pnas.2102698118 (2021).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Ospelt, C. et al. Overexpression of toll-like receptors 3 and 4 in synovial tissue from patients with early rheumatoid arthritis: toll-like receptor expression in early and longstanding arthritis. Arthritis Rheum. 58, 3684–3692 (2008).

    Article 
    CAS 
    PubMed 

    Google Scholar
     

  • Mizoguchi, F. et al. Functionally distinct disease-associated fibroblast subsets in rheumatoid arthritis. Nat. Commun. 9, 789 (2018).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Nygaard, G. & Firestein, G. S. Restoring synovial homeostasis in rheumatoid arthritis by targeting fibroblast-like synoviocytes. Nat. Rev. Rheumatol. 16, 316–333 (2020).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Chang, S. K. et al. Cadherin-11 regulates fibroblast inflammation. Proc. Natl Acad. Sci. USA 108, 8402–8407 (2011).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Noss, E. H., Chang, S. K., Watts, G. F. & Brenner, M. B. Modulation of matrix metalloproteinase production by rheumatoid arthritis synovial fibroblasts after cadherin 11 engagement. Arthritis Rheum. 63, 3768–3778 (2011).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Lee, D. M. et al. Cadherin-11 in synovial lining formation and pathology in arthritis. Science 315, 1006–1010 (2007).

    Article 
    CAS 
    PubMed 

    Google Scholar
     

  • Lee, A. et al. Tumor necrosis factor α induces sustained signaling and a prolonged and unremitting inflammatory response in rheumatoid arthritis synovial fibroblasts. Arthritis Rheum. 65, 928–938 (2013).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Sohn, C. et al. Prolonged tumor necrosis factor α primes fibroblast-like synoviocytes in a gene-specific manner by altering chromatin. Arthritis Rheumatol. 67, 86–95 (2015).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Ospelt, C., Gay, S. & Klein, K. Epigenetics in the pathogenesis of RA. Semin. Immunopathol. 39, 409–419 (2017).

    Article 
    PubMed 

    Google Scholar
     

  • Ai, R. et al. Comprehensive epigenetic landscape of rheumatoid arthritis fibroblast-like synoviocytes. Nat. Commun. 9, 1921 (2018).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Yan, M. et al. ETS1 governs pathological tissue-remodeling programs in disease-associated fibroblasts. Nat. Immunol. 23, 1330–1341 (2022).

    Article 
    CAS 
    PubMed 

    Google Scholar
     

  • Friščić, J. et al. The complement system drives local inflammatory tissue priming by metabolic reprogramming of synovial fibroblasts. Immunity 54, 1002–1021.e1010 (2021).

    Article 
    PubMed 

    Google Scholar
     

  • Koedderitzsch, K., Zezina, E., Li, L., Herrmann, M. & Biesemann, N. TNF induces glycolytic shift in fibroblast like synoviocytes via GLUT1 and HIF1A. Sci. Rep. 11, 19385 (2021).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Friščić, J. et al. Reset of inflammatory priming of joint tissue and reduction of the severity of arthritis flares by bromodomain inhibition. Arthritis Rheumatol. https://doi.org/10.1002/art.42378 (2022).

    Article 

    Google Scholar
     



  • Source link

    Related Articles

    Leave a Reply

    Stay Connected

    9FansLike
    4FollowersFollow
    0SubscribersSubscribe
    - Advertisement -spot_img

    Latest Articles

    %d bloggers like this: