Abstract: TH-PO0696
γδ T Cells' Role in a Murine Model of Glomerulosclerosis
Session Information
- Glomerular Diseases: Immunopathogenesis and Targeted Therapeutics
November 06, 2025 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Glomerular Diseases
- 1401 Glomerular Diseases: Mechanisms, including Podocyte Biology
Authors
- Cocchini, Lorenzo, Icahn School of Medicine at Mount Sinai, New York, New York, United States
- Bigatti, Carolina, Icahn School of Medicine at Mount Sinai, New York, New York, United States
- Cravedi, Paolo, Icahn School of Medicine at Mount Sinai, New York, New York, United States
Background
Focal segmental glomerulosclerosis (FSGS) is a significant cause of nephrotic syndrome and chronic kidney disease. Gamma delta (γδ) T cells are a subset of unconventional T cells that have been implicated in various immune responses. Few studies analyzed their function in FSGS.
Methods
We induced FSGS in wild type (WT) C57BL/6 (B6) and BALB/c male by injecting Adriamycin (ADR) at 20 mg/kg and 10mg/kg, respectively. To test the effect of γδ T cells, we treated mice at the time of ADR injection with UC7-13D5 monoclonal antibody (Ab) anti-γδ T cell receptor (TCR) or isotype control antibody. We analyzed the urinary albumin to creatinine ratio (ACR) every week for 5 weeks. Two-way ANOVA and t-test were applied to analyze the data.
Results
Upon ADR injection, γδ T cell in the kidney significantly increased compared to mice not receiving ADR (p = 0.0489). Mice treated with the UC7-13D5 Ab developed significantly higher ACR in both B6 and BALB/c mice (Figure 1). BUN, cholesterol and albumin in the serum were not significantly altered compared to basal values and no significant differences were found between groups.
Conclusion
Our data support a pathogenic role of γδ T cells in FSGS. However, the exact biological effects of UC7-13D5 remain unclear. Some authors have suggested that the UC7-13D5 antibody activates γδ T cells, but further studies are needed to better understand the role of γδ T cells in FSGS pathophysiology.