Contribution of plasma cells and B cells to hidradenitis suppurativa pathogenesis

Johann E. Gudjonsson, Lam C. Tsoi, Feiyang Ma, Allison C. Billi, K. R. van Straalen, A. R.J.V. Vossen, H. H. van der Zee, Paul W. Harms, Rachael Wasikowski, Christine M. Yee, Syed M. Rizvi, Xianying Xing, Enze Xing, Olesya Plazyo, Chang Zeng, Matthew T. Patrick, Margaret M. Lowe, Richard E. Burney, Jeffrey H. Kozlow, Jill R. Cherry-BukowiecYanyun Jiang, Joseph Kirma, Stephan Weidinger, Kelly C. Cushing, Michael D. Rosenblum, Celine Berthier, Amanda S. MacLeod, John J. Voorhees, Fei Wen, J. Michelle Kahlenberg, Emanual Maverakis, Robert L. Modlin, Errol P. Prens

Research output: Contribution to journalArticlepeer-review

33 Scopus citations


Hidradenitis suppurativa (HS) is a debilitating chronic inflammatory skin disease characterized by chronic abscess formation and development of multiple draining sinus tracts in the groin, axillae, and perineum. Using proteomic and transcriptomic approaches, we characterized the inflammatory responses in HS in depth, revealing immune responses centered on IFN-γ, IL-36, and TNF, with lesser contribution from IL-17A. We further identified B cells and plasma cells, with associated increases in immunoglobulin production and complement activation, as pivotal players in HS pathogenesis, with Bruton's tyrosine kinase (BTK) and spleen tyrosine kinase (SYK) pathway activation as a central signal transduction network in HS. These data provide preclinical evidence to accelerate the path toward clinical trials targeting BTK and SYK signaling in moderate-to-severe HS.

Original languageEnglish (US)
Article number139930
JournalJCI Insight
Issue number19
StatePublished - Oct 2 2020

ASJC Scopus subject areas

  • Medicine(all)


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