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Mass cytometry uncovers a distinct peripheral immune profile and upregulated CD38 expression in patients with hidradenitis suppurativa

Cellular & Molecular Immunology volume 20, pages 972–975 (2023)Cite this article

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Hidradenitis suppurativa (HS) is a chronic inflammatory skin disease with a worldwide prevalence of 0.3–4.0%, wherein abscesses and dermal sinus tracts form in intertriginous skin [1]. HS remains poorly treated due to a lack of knowledge regarding its immunopathogenesis [2]. Recent study findings have implicated multiple immune pathways and effector molecules underlying HS pathophysiology [2]. Increased circulating inflammatory proteins, autoantibodies, and extracellular matrix degradation products highlight that systemic inflammation is a feature of the disease [2,3,4]. Circulating immune cells serve as a good proxy for disease severity and risk in other inflammatory conditions [5]; however, an unbiased characterization of the changes in the peripheral immunome of patients with HS has not been reported and is desperately needed. Cytometry by time-of-flight (CyTOF) enables highly parametric immune profiling, which led to the discovery of disease-associated immunome signatures and cellular effectors in other inflammatory diseases [5].

In this study, we characterized the immune profile of fresh whole-blood samples from a cohort of 18 patients with HS and 11 healthy controls (HCs) (Supplementary Fig. S1A and Supplementary Table S1) using a standardized 30-marker whole-blood immunome profiling panel (Supplementary Table S2) that can identify 33 immune cell populations (Supplementary Table S3). Bivariate gating and marker expression showed good separation of major immune clusters in tSNEs (Supplementary Fig. S1B, C).

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Fig. 1

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Acknowledgements

We would like to acknowledge the patients who donated to our study. We recognize that without them, this work would be impossible, and the privilege is to be able to serve them in this capacity. We hope that through our continued efforts, we will relieve the burden of their disease. We would like to thank Yi Yao for providing advice on the analysis of CyTOF data. We would also like to acknowledge the members of the Mi Laboratory and HFHS Department of Dermatology for their continued support of our work. This study was funded by NIH/NIAMS (R01AR078688 to Q-SM and WL, R21AR079089 to Q-SM and IA) and the Henry Ford Immunology Program (T71016 to Q-SM and T71017 to LZ).

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Authors and Affiliations

  1. Center for Cutaneous Biology and Immunology Research, Department of Dermatology, Henry Ford Health System, Detroit, MI, 48202, USA

    Peter Dimitrion, Iltefat Hamzavi, Congcong Yin, Jugmohit Toor, Kalpana Subedi, Namir Khalasawi, Angela Miller, Richard Huggins, Indra Adrianto, Jesse Veenstra, Gautham Vellaichamy, Aakash Hans, Henry Lim, David Ozog, Li Zhou & Qing-Sheng Mi

  2. Immunology Research Program, Henry Ford Cancer Institute, Henry Ford Health System, Detroit, MI, 48202, USA

    Peter Dimitrion, Congcong Yin, Jugmohit Toor, Kalpana Subedi, Namir Khalasawi, Indra Adrianto, Jesse Veenstra, Aakash Hans, Li Zhou & Qing-Sheng Mi

  3. Cancer Biology Graduate Program, School of Medicine, Wayne State University, Detroit, MI, 48202, USA

    Peter Dimitrion, Jugmohit Toor & Qing-Sheng Mi

  4. Center for Bioinformatics, Department of Public Health Sciences, Henry Ford Health System, Detroit, MI, 48202, USA

    Indra Adrianto

  5. Department of Dermatology, Wayne State University School of Medicine, Detroit, MI, 48202, USA

    Steven Daveluy

  6. University of Alabama at Birmingham (UAB) Research Center of Excellence in Arsenicals, Department of Dermatology, University of Alabama at Birmingham, Birmingham, AL, USA

    Mohammad Athar

  7. Department of Dermatology, University of California San Francisco, San Francisco, CA, USA

    Wilson Liao

  8. Department of Biochemistry, Microbiology, and Immunology, School of Medicine, Wayne State University, Detroit, MI, 48202, USA

    Li Zhou & Qing-Sheng Mi

Authors
  1. Peter Dimitrion
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Contributions

PD participated in patient recruitment and experimental design; performed research; collected, analyzed, and interpreted data; performed statistical analysis; and drafted and revised the manuscript. IH participated in patient recruitment and experimental design; performed research; and revised the manuscript. CY participated in patient recruitment and data collection. IL analyzed and performed statistical analysis for high-dimensional imaging data and revised the manuscript. JT, KS, and NK collected data and revised the manuscript. AM, RH, GV, and AH participated in patient recruitment. JV participated in data collection, analysis and interpretation and manuscript revisions. SD, MA, WL, HL, and DO participated in manuscript revisions. LZ and Q-SM supervised all aspects of the work; acquired funding and resources; and participated in data analysis and interpretation, manuscript drafting, and manuscript revisions.

Corresponding authors

Correspondence to Li Zhou or Qing-Sheng Mi.

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Competing interests

IH has served as an investigator (grant to institution) for Pfizer Inc, Bayer, Lenicura, Incyte, Estee Lauder, L’Oreal, Unigen, Avita, Arcutis Biotherapeutics, and Ferndale Laboratories, Inc.; as an Advisory Board member for AbbVie; and as a consultant to Galderma Laboratories, LP, Incyte, Pfizer, UCB, Boehringer Ingelheim, Beiersdorf, and Clarify Medical. RH is a principal investigator for Pfizer, Incyte, Arcutis and the Immune Tolerance Network. WL has received research grant funding from AbbVie, Amgen, Janssen, Leo, Novartis, Pfizer, Regeneron, and TRex Bio. HL is an investigator for Incyte, L’Oreal, Pfizer, and PCORI; has served as a consultant for Pierre Fabre, ISDIN, Ferndale, La Roche-Posay, Cantabria, and Beiersdorf; and has participated as a speaker in general educational sessions for La Roche-Posay and Cantabria Labs. All other authors have no conflicts of interest to report.

Ethics approval

These procedures and protocols were approved by the Henry Ford Health Institutional Review Board (IRB# 12826).

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Dimitrion, P., Hamzavi, I., Yin, C. et al. Mass cytometry uncovers a distinct peripheral immune profile and upregulated CD38 expression in patients with hidradenitis suppurativa. Cell Mol Immunol 20, 972–975 (2023). https://doi.org/10.1038/s41423-023-01037-6

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