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Bullous Pemphigoid Develops Independently of DAP12.

Manuela Pigors1, Sabrina Patzelt1, Maëlys Brudey1

  • 1Lübeck Institute of Experimental Dermatology, University of Lübeck, 23562 Lübeck, Germany.

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|November 27, 2025
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Summary

The DNAX-activating protein of 12 kDa (DAP12) pathway does not significantly impact bullous pemphigoid (BP) disease activity, despite modulating immune cell composition in experimental models. DAP12 signaling does not drive this autoimmune blistering disease.

Keywords:
PI3KTREM1TREM2autoimmune blistering diseasebasement membrane zoneparsaclisibtype XVII collagentyrobp

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Area of Science:

  • Immunology
  • Dermatology
  • Autoimmunity

Background:

  • DNAX-activating protein of 12 kDa (DAP12) is crucial in innate immunity but its role in autoimmunity is complex.
  • Bullous pemphigoid (BP) is a common autoimmune blistering disease with unclear underlying mechanisms.

Purpose of the Study:

  • To investigate the role of the DAP12 pathway in experimental bullous pemphigoid.
  • To determine if DAP12 signaling influences disease activity and immune cell infiltration in BP.

Main Methods:

  • A mouse model of bullous pemphigoid was induced by anti-type XVII collagen (Col17) IgG transfer.
  • Flow cytometry and immunofluorescence were used to analyze lesional skin and immune cell populations.
  • Pharmacological inhibition of PI3Kδ, a downstream kinase, was assessed.

Main Results:

  • DAP12-deficient and wildtype mice exhibited comparable disease activity, indicating DAP12 independence.
  • TREM1 was upregulated in wildtype BP lesions, while TREM2+ cells were reduced in both wildtype and DAP12-deficient mice compared to controls.
  • DAP12 deficiency altered inflammatory infiltrates, reducing eosinophil frequencies.

Conclusions:

  • The DAP12/TREM1/2 axis does not significantly influence overall disease activity in experimental bullous pemphigoid.
  • DAP12 signaling modulates local immune cell composition but is not essential for disease induction or progression in this model.