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Peer-reviewedCC BY 4.0International Journal of Molecular Sciences

Bruton Tyrosine Kinase Inhibitors in Immune-Mediated Skin Diseases: Current Evidence and Future Directions

  • Zihan Wang1
  • Junchen He1
  • Ting Zhang1
  • Jiayu Peng1
  • Lulu Xie1
  • Bingrun Li2
  • Cunhao Shan2
  • Litao Zhang1
  • Zuotao Zhao1
  1. 1Institute of Dermatology, Tianjin Academy of Traditional Chinese Medicine, Tianjin 300120, China
  2. 2Graduate School, Tianjin University of Traditional Chinese Medicine, Tianjin 301617, China
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Abstract

Bruton tyrosine kinase (BTK) is a central signaling molecule that links the B-cell receptor (BCR), Fc receptors, and Toll-like receptors (TLRs). By coordinating signaling in B cells, mast cells, macrophages, and other immune cells, BTK occupies an important position in cutaneous immune responses. BTK inhibitors (BTKis) can inhibit B-cell and Fc-receptor-dependent effector-cell signaling, providing a mechanistic rationale for several immune-mediated skin diseases. However, these cellular effects should not be equated with suppression of established autoantibody production or durable disease modification. This review summarizes the biological functions of BTK and critically evaluates clinical and translational evidence in chronic spontaneous urticaria (CSU), atopic dermatitis (AD), pemphigus, psoriasis, and hidradenitis suppurativa (HS). Evidence is strongest for short-term symptom control in CSU cases. Clinical value remains uncertain in pemphigus and HS, rilzabrutinib did not meet its primary AD efficacy endpoint and topical atuzabrutinib showed no exploratory efficacy benefit, and psoriasis evidence is preclinical. Priorities include prospective validation of predictive biomarkers, disease-specific confirmatory trials, agent- and setting-specific safety assessments, and long-term and real-world follow-up.

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Cite

BibTeXRIS
BibTeX
@article{wang2026bruton,
  title = {{Bruton Tyrosine Kinase Inhibitors in Immune-Mediated Skin Diseases: Current Evidence and Future Directions}},
  author = {Zihan Wang and Junchen He and Ting Zhang and Jiayu Peng and Lulu Xie and Bingrun Li and Cunhao Shan and Litao Zhang and Zuotao Zhao},
  journal = {International Journal of Molecular Sciences},
  year = {2026},
  month = oct,
  doi = {10.3390/ijms27209375},
  url = {https://www.mdpi.com/1422-0067/27/20/9375},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Bruton Tyrosine Kinase Inhibitors in Immune-Mediated Skin Diseases: Current Evidence and Future Directions
AU  - Zihan Wang
AU  - Junchen He
AU  - Ting Zhang
AU  - Jiayu Peng
AU  - Lulu Xie
AU  - Bingrun Li
AU  - Cunhao Shan
AU  - Litao Zhang
AU  - Zuotao Zhao
PY  - 2026
DA  - 2026/10/21
JO  - International Journal of Molecular Sciences
DO  - 10.3390/ijms27209375
UR  - https://www.mdpi.com/1422-0067/27/20/9375
AB  - Bruton tyrosine kinase (BTK) is a central signaling molecule that links the B-cell receptor (BCR), Fc receptors, and Toll-like receptors (TLRs). By coordinating signaling in B cells, mast cells, macrophages, and other immune cells, BTK occupies an important position in cutaneous immune responses. BTK inhibitors (BTKis) can inhibit B-cell and Fc-receptor-dependent effector-cell signaling, providing a mechanistic rationale for several immune-mediated skin diseases. However, these cellular effects should not be equated with suppression of established autoantibody production or durable disease modification. This review summarizes the biological functions of BTK and critically evaluates clinical and translational evidence in chronic spontaneous urticaria (CSU), atopic dermatitis (AD), pemphigus, psoriasis, and hidradenitis suppurativa (HS). Evidence is strongest for short-term symptom control in CSU cases. Clinical value remains uncertain in pemphigus and HS, rilzabrutinib did not meet its primary AD efficacy endpoint and topical atuzabrutinib showed no exploratory efficacy benefit, and psoriasis evidence is preclinical. Priorities include prospective validation of predictive biomarkers, disease-specific confirmatory trials, agent- and setting-specific safety assessments, and long-term and real-world follow-up.
SN  - 1422-0067
ER  -