Case report: Low-dose interleukin-2: a treatment of bullous pemphigoid with predominantly perifollicular blistering caused by PD-1/PD-L1 inhibitor

Front Immunol. 2024 Dec 10:15:1496413. doi: 10.3389/fimmu.2024.1496413. eCollection 2024.

Abstract

Objectives: This study aimed to evaluate the efficacy of low-dose interleukin (IL-2) treatment for bullous pemphigoid (BP) caused by anti-programmed cell death protein 1/ligand 1 (PD-1/PD-L1) inhibitors.

Methods: Low-dose IL-2 treatment was standardized for BP. The Bullous Pemphigoid Disease Area Index (BPDAI), 5D-Itch Scale (5D-IS), and Dermatology Life Quality Index (DLQI) were recorded before and after treatment, and hexachromatic lymphocytes, regulatory T cells (Treg cells), and cytokines were measured.

Results: A significant decline in the BPDAI score, 5D-IS, and DLQI score was observed following treatment. The count of B-cells, CD4+ T-cells, CD8+ T-cells, Treg cells, and the levels of cytokines (IL-4, -8, and -10) were significantly downregulated in comparison to baseline measurements.

Conclusion: Low-dose IL-2 could be an effective therapeutic choice for treating BP caused by PD-1/PD-L1 inhibitors.

Keywords: Low-dose IL-2; PD-1/PD-L1 inhibitor; bullous pemphigoid; immunotherapy; perifollicular blistering.

Publication types

  • Case Reports

MeSH terms

  • Aged
  • B7-H1 Antigen* / antagonists & inhibitors
  • Cytokines / metabolism
  • Female
  • Humans
  • Immune Checkpoint Inhibitors* / administration & dosage
  • Immune Checkpoint Inhibitors* / adverse effects
  • Immune Checkpoint Inhibitors* / therapeutic use
  • Interleukin-2*
  • Male
  • Pemphigoid, Bullous* / drug therapy
  • Pemphigoid, Bullous* / immunology
  • Programmed Cell Death 1 Receptor* / antagonists & inhibitors
  • T-Lymphocytes, Regulatory / drug effects
  • T-Lymphocytes, Regulatory / immunology
  • Treatment Outcome

Substances

  • Interleukin-2
  • Programmed Cell Death 1 Receptor
  • Immune Checkpoint Inhibitors
  • B7-H1 Antigen
  • CD274 protein, human
  • PDCD1 protein, human
  • Cytokines

Grants and funding

The author(s) declare financial support was received for the research, authorship, and/or publication of this article. This work was supported by grants from National Natural Science Foundation of China (No. 82360624).