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Single-cell sequencing reveals Hippo signaling as a driver of fibrosis in hidradenitis suppurativa

  • Kelsey R. van Straalen
  • , Feiyang Ma
  • , Pei Suen Tsou
  • , Olesya Plazyo
  • , Mehrnaz Gharaee-Kermani
  • , Marta Calbet
  • , Xianying Xing
  • , Mrinal K. Sarkar
  • , Ranjitha Uppala
  • , Paul W. Harms
  • , Rachael Wasikowski
  • , Lina Nahlawi
  • , Mio Nakamura
  • , Milad Eshaq
  • , Cong Wang
  • , Craig Dobry
  • , Jeffrey H. Kozlow
  • , Jill Cherry-Bukowiec
  • , William D. Brodie
  • , Kerstin Wolk
  • Özge Uluçkan, Megan N. Mattichak, Matteo Pellegrini, Robert L. Modlin, Emanual Maverakis, Robert Sabat, J. Michelle Kahlenberg, Allison C. Billi, Lam C. Tsoi, Johann E. Gudjonsson*
*Corresponding author for this work
  • University of Michigan, Ann Arbor
  • Almirall, S.A
  • Charité – Universitätsmedizin Berlin
  • University of California at Los Angeles
  • University of California at Davis

Research output: Contribution to journalArticleAcademicpeer-review

41 Citations (Scopus)
96 Downloads (Pure)

Abstract

Hidradenitis suppurativa (HS) is a chronic inflammatory disease characterized by abscesses, nodules, dissecting/draining tunnels, and extensive fibrosis. Here, we integrate single-cell RNA sequencing, spatial transcriptomics, and immunostaining to provide an unprecedented view of the pathogenesis of chronic HS, characterizing the main cellular players and defining their interactions. We found a striking layering of the chronic HS infiltrate and identified the contribution of 2 fibroblast subtypes (SFRP4+ and CXCL13+) in orchestrating this compartmentalized immune response. We further demonstrated the central role of the Hippo pathway in promoting extensive fibrosis in HS and provided preclinical evidence that the profibrotic fibroblast response in HS can be modulated through inhibition of this pathway. These data provide insights into key aspects of HS pathogenesis with broad therapeutic implications.

Original languageEnglish
Article numbere169225
JournalJournal of Clinical Investigation
Volume134
Issue number3
DOIs
Publication statusPublished - 1 Feb 2024

Bibliographical note

Publisher Copyright: © 2023, van Straalen et al.

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