# Regulatory T cell therapy for myeloperoxidase-specific anti-neutrophil cytoplasmic antibody associated vasculitis

**Authors:** Elean S. V. Tay, Yi T. Ting, Poh-Yi Gan, Joshua D. Ooi

PMC · DOI: 10.3389/fimmu.2025.1675251 · Frontiers in Immunology · 2025-11-03

## TL;DR

This paper reviews the potential of using regulatory T cell therapy to treat a rare autoimmune disease called MPO-associated vasculitis, aiming to reduce reliance on toxic steroids.

## Contribution

The paper explores the novel use of genetically engineered regulatory T cells to target the root cause of MPO-associated vasculitis.

## Key findings

- MPO-AAV has a poor prognosis and often leads to end-stage renal failure despite current treatments.
- Regulatory T cell therapy shows promise as a targeted, less toxic treatment option for AAV.
- Genetic and epigenetic factors may influence the development of MPO-AAV, particularly in certain populations.

## Abstract

Anti-neutrophil cytoplasmic antibodies (ANCA)-associated vasculitis (AAV) is a rare autoimmune disease characterized by the inflammation of small vessels. It is most commonly caused by ANCA targeting proteinase 3 (PR3) and myeloperoxidase (MPO) which are found in neutrophil lysosomes. The most common affected organs are respiratory tracts and kidneys, though other organs can be involved too. Although the cause of disease between PR3-AAV and MPO-AAV is similar, they vary in pathogenesis. Epigenetic and genetic factors may play a role in the disease development as certain population such as Chinese with HLA-DRB1*04:05 are more prevalent in MPO-AAV patient population. The prognosis for them is usually poor, often resulting in end-stage renal failure even with existing treatment. Current treatment for AAV relies heavily on corticosteroids which are toxic for long-term usage. Hence, there is a strong need to develop new, less toxic and targeted therapy for this disease. Regulatory T cell (Treg) therapy is a new type of therapy with the potential to specifically re-establish tolerance to the target autoantigen (MPO or PR3). This review will delve into the pathogeneses of AAV and discuss the potential of using genetically engineered Tregs to treat the cause of disease.

## Linked entities

- **Proteins:** MPO (myeloperoxidase), PRTN3 (proteinase 3), ancA (ADP/ATP translocase)
- **Diseases:** AAV (MONDO:0015492), end-stage renal failure (MONDO:0004375)

## Full-text entities

- **Genes:** MPO (myeloperoxidase) [NCBI Gene 4353], PRTN3 (proteinase 3) [NCBI Gene 5657] {aka ACPA, AGP7, C-ANCA, CANCA, MBN, MBT}, HLA-DRB1 (major histocompatibility complex, class II, DR beta 1) [NCBI Gene 3123] {aka DRB1, HLA-DR1B, HLA-DRB, SS1}
- **Diseases:** AAV (MESH:D014657), Anti-neutrophil cytoplasmic antibodies (ANCA)-associated vasculitis (MESH:D056648), inflammation (MESH:D007249), end-stage renal failure (MESH:D007676), autoimmune disease (MESH:D001327)
- **Chemicals:** anti (-)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12620468/full.md

## References

111 references — full list in the complete paper: https://tomesphere.com/paper/PMC12620468/full.md

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Source: https://tomesphere.com/paper/PMC12620468