Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Editorial
. 2023 Jan 10:9:1129021.
doi: 10.3389/fmed.2022.1129021. eCollection 2022.

Editorial: The kidney in auto-immune and auto-inflammatory processes: Definitions, mechanisms, and biomarkers

Augusto Vaglio  1   2 , Marco Gattorno  3 , Stephen McAdoo  4   5 , Laura Piera Obici  6 , Gian Marco Ghiggeri  7
Affiliations
Editorial

Editorial: The kidney in auto-immune and auto-inflammatory processes: Definitions, mechanisms, and biomarkers

Augusto Vaglio et al. Front Med (Lausanne). .
No abstract available

Keywords: ANCA associated vasculitis; IgA vasculitis; amyloidosis; autoimmune renal diseases; autoinflammatory diseases; lupus nephritis; membranous nephropathy.

PubMed Disclaimer

Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
Most of the immune-mediated, systemic diseases that affect the kidney are “complex diseases” that result from the interaction between genetic susceptibility factors and environmental factors. The pathogenic mechanisms through which they cause kidney disease involve T-cell and macrophage/dendritic cell-mediated immunity, neutrophil activation and NET (neutrophil extracellular trap) formation with the exposure of auto-antigens and the consequent stimulation of autoimmune responses, the production of autoantibodies and the secretion of immuno-modulatory cytokines. The diseases included in this spectrum may have well-known pathogenic autoantibodies (e.g., lupus nephritis, ANCA-associated vasculitis, membranous nephropathy- all highlighted in yellow), pathogenic immune-complexes (IgA nephropathy, highlighted in blue), pathogenic monoclonal or polyclonal proteins able to form amyloid (amyloidosis, in orange), autoinflammatory or yet unknown pathogenic hallmarks (all the conditions highlighted in gray).
See this image and copyright information in PMC

Comment on

  • Editorial on the Research Topic The kidney in auto-immune and auto-inflammatory processes: Definitions, mechanisms, and biomarkers

References

    1. Dedong H, Feiyan Z, Jie S, Xiaowei L, Shaoyang W. Analysis of interleukin-17 and interleukin-23 for estimating disease activity and predicting the response to treatment in active lupus nephritis patients. Immunol Lett. (2019) 210:33–9. 10.1016/j.imlet.2019.04.002 - DOI - PubMed
    1. Paust H-J, Turner J-E, Steinmetz OM, Peters A, Heymann F, Hölscher C, et al. The IL-23/Th17 axis contributes to renal injury in experimental glomerulonephritis. J Am Soc Nephrol. (2009) 20:969–79. 10.1681/ASN.2008050556 - DOI - PMC - PubMed
    1. van Vollenhoven RF, Hahn BH, Tsokos GC, Wagner CL, Lipsky P, Touma Z, et al. Efficacy and safety of ustekinumab, an IL-12 and IL-23 inhibitor, in patients with active systemic lupus erythematosus: results of a multicentre, double-blind, phase 2, randomised, controlled study. Lancet. (2018) 392:1330–9. 10.1016/S0140-6736(18)32167-6 - DOI - PubMed
    1. Krzewski K, Gil-Krzewska A, Nguyen V, Peruzzi G, Coligan JE. LAMP1/CD107a is required for efficient perforin delivery to lytic granules and NK-cell cytotoxicity. Blood. (2013) 121:4672–83. 10.1182/blood-2012-08-453738 - DOI - PMC - PubMed
    1. Nathan C. Neutrophils and immunity: challenges and opportunities. Nat Rev Immunol. (2006) 6:173–82. 10.1038/nri1785 - DOI - PubMed

Publication types