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STING Drives CD4+T Cell Differentiation via JAK-STAT Signalling in Bullous Pemphigoid
Weiwei Jiang1, Mengke Sun2,3, Junchen He1
1Department of Dermatology, Tianjin Institute of Integrative Dermatology, Tianjin Academy of Traditional Chinese Medicine Affiliated Hospital, Tianjin, China.
Experimental Dermatology
|July 17, 2026
Summary
Stimulator of interferon genes (STING) is upregulated in bullous pemphigoid (BP) skin. Inhibiting STING calms immune pathways in CD4+ T cells, suggesting STING as a therapeutic target for this autoimmune blistering disease.
Area of Science:
- Immunology
- Dermatology
- Molecular Biology
Background:
- Bullous pemphigoid (BP) is an autoimmune blistering disease with increasing incidence.
- The immune mechanisms underlying BP pathogenesis are not fully understood.
- Stimulator of interferon genes (STING) is a key signaling molecule in immunity, implicated in other autoimmune conditions.
Purpose of the Study:
- To investigate the role of STING in bullous pemphigoid.
- To explore the impact of STING on CD4+ T cell responses in BP.
- To identify potential therapeutic targets for BP.
Main Methods:
- Compared STING expression in lesional skin of BP patients and healthy controls.
- Performed transcriptomic analysis on peripheral blood CD4+ T cells from BP patients.
- Utilized a STING inhibitor (C176) to assess its effects on signaling pathways and gene expression.
Main Results:
- STING expression was significantly elevated in BP lesional skin.
- CD4+ T cells in BP patients showed enrichment in JAK-STAT signaling, T cell activation, and type I interferon pathways.
- Pharmacological inhibition of STING reduced aberrant signaling and suppressed elevated STING1, JAK1, and CXCR5 mRNA levels.
Conclusions:
- STING contributes to bullous pemphigoid immunopathogenesis.
- STING regulates the JAK-STAT signaling axis and promotes abnormal CD4+ T cell activation in BP.
- STING represents a potential therapeutic target for bullous pemphigoid.
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