Study of cytokine-induced immunity in bullous pemphigoid: recent developments

Abstract

Bullous pemphigoid (BP) is an organ-specific disease. Its pathogenesis has not been clearly studied yet; However, studies in recent years have shown that its pathogenesis is related to T helper cells. The pathogenesis of BP is mainly related to Th2 and Th17-related cytokines. IL-4, IL-5 and IL-13 cause eosinophil recruitment, promote antibody production, trigger pruritus and promote blister formation and other symptoms. IL-17 and IL-23 promote the production of matrix metalloproteinase-9 (MMP-9) by related cells, which causes dermo-epidermal junction (DEJ) separation to form bullae and blisters, and can persist in BP inflammation. The serum concentrations of IL-17 and IL-23 are related to the prognosis of BP. In this paper, we focus on the role of related cytokines in the pathogenesis of bullous pemphigoid and the relationship between the related cytokine populations secreted by three major T helper cells—helper T lymphocytes 1 (Th1), Th2, and Th17. A better understanding of the biological and immunological functions of cytokines associated with BP patients will provide opportunities for therapeutic targets in BP.

Keywords:

• Bullous pemphigoid
• cytokines
• interferon-γ
• interleukin-4
• Th1 cells
• Th2 cells
• Th17 cells

Acknowledgements

We would like to acknowledge the hard and dedicated work of all the staff that implemented the intervention and evaluation components of the study.

Author contributions

Conception and design of the research: Ruiting Huang and Fuqiong Jiang. Acquisition of data: Ruiting Huang, Lingyu Hu and Fuqiong Jiang. Analysis and interpretation of the data: Ruiting Huang. Statistical analysis: Ruiting Huang, Lingyu Hu and Fuqiong Jiang. Obtaining financing: Ruiting Huang and Fuqiong Jiang. Writing of the manuscript: Ruiting Huang and Fuqiong Jiang. Critical revision of the manuscript for intellectual content: Fuqiong Jiang, Ruiting Huang and Lingyu Hu. All authors read and approved the final draft.

Disclosure statement

The authors declare that they have no competing interests.

Data availability statement

The datasets used and/or analysed during the current study available from the corresponding author on reasonable request.

Additional information

Funding

This work is supported by the Postgraduate Innovation Fund of Kunming Medical University 2022 (No. 2022S283), Science and Technology Fund of Yunnan Province: 202301AY070001-248, and Clinical Research Fund of the Second Affiliated Hospital of Kunming Medical University: ynllT2022006.