ASN's Mission

To create a world without kidney diseases, the ASN Alliance for Kidney Health elevates care by educating and informing, driving breakthroughs and innovation, and advocating for policies that create transformative changes in kidney medicine throughout the world.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005

email@asn-online.org

202-640-4660

The Latest on X

Kidney Week

Abstract: FR-PO825

Establishment of Human IgG Autoantibodies Derived from Patients with Lupus Nephritis and Deposition of Resultant Human IgG-Containing Immune Complexes in the Kidney and Skin of Mice

Session Information

Category: Glomerular Diseases

  • 1401 Glomerular Diseases: Mechanisms, including Podocyte Biology

Authors

  • Ka, Shuk-Man, Department of Medicine, National Defense Medical Center, Taipei, Taiwan
  • Chen, Ann, Department of Pathology, Hualien Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Hualien, Taiwan
Background

In Taiwan, lupus nephritis (LN) has a trend of 4.3–13.4% rate of progression to end-stage renal disease (ESRD). Treatment for LN mainly relies on glucocorticoids and other immunosuppressants, but targeting more specific pathogenic molecules from the upstream pathways involved in the development and progression of the disease, e.g., etiological autoantibodies (autoAbs), is crucial and remains a unmet medical need.

Methods

We have recently established a human hybridoma platform to generate two human IgG against dsDNA autoantibodies (autoAbs) using peripheral blood mononuclear cells (PBMCs) from LN patients (LiuK-NDMC-01 and LiuK-NDMC-02) to which we performed sequencing and tests for capacity of inducing inflammatory responses and deposition of immune complexes (ICs) in the kidney and skin of ASID mice that mimics the human disease.

Results

By injecting intravenously a single dose of the LiuK-NDMC-01 autoAb against dsDNA and human dsDNA extracted from a human THP-1 monocyte cell line, renal deposition of the human IgG-containing ICs in ASID mice was induced. Immunofluorescence examination showed deposition of human IgG and C3 diffusely in the kidney and IgG in the skin. This effect was also confirmed by a Western blot analysis using renal proteins extracted from the ASID mice. Moreover, increased NLRP3 inflammasome-mediated IL-1β secretion was observed in human macrophages that were primed with the ICs containing the LiuK-NDMC-01 autoAb and dsDNA compared with saline-control counterparts.

Conclusion

Collectively, two new human IgG autoantibodies were established using PBMCs from LN patients. One of these human IgG autoAb was further validated for deposition of the IgG-containing ICs in both the kidney and skin, mimicking LN patients. The ICs was shown to induce inflammatory reaction as demonstrated by resultant activation of NLRP3 inflammasome and subsequent IL-1β secretion in human macrophages.

Funding

  • Government Support – Non-U.S.