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1 Department of Microbiology and Immunology, Emory University School of Medicine, Atlanta, GA 30322, USA.
2 Department of Microbiology and Immunology, Emory University School of Medicine, Atlanta, GA 30322, USA; Department of Dermatology, Emory University School of Medicine, Atlanta, GA 30322, USA; Winship Cancer Institute, Emory University School of Medicine, Atlanta, GA 30322, USA. Electronic address: chaoran.li@emory.edu.
1 Department of Microbiology and Immunology, Emory University School of Medicine, Atlanta, GA 30322, USA.
2 Department of Microbiology and Immunology, Emory University School of Medicine, Atlanta, GA 30322, USA; Department of Dermatology, Emory University School of Medicine, Atlanta, GA 30322, USA; Winship Cancer Institute, Emory University School of Medicine, Atlanta, GA 30322, USA. Electronic address: chaoran.li@emory.edu.
Hidradenitis suppurativa (HS) is a severe chronic inflammatory skin disease with limited response to therapy. In this issue of Immunity, Yu et al.1 identify skin tertiary lymphoid structures (TLSs) as primary sites for lymphocyte clonal expansion and autoantibody production, driving disease progression, and provide insight into how formation and maintenance of TLS impact therapeutic outcomes.
Yu WW, Barrett JNP, Tong J, Lin MJ, Marohn M, Devlin JC, Herrera A, Remark J, Levine J, Liu PK, Fang V, Zellmer AM, Oldridge DA, Wherry EJ, Lin JR, Chen JY, Sorger P, Santagata S, Krueger JG, Ruggles KV, Wang F, Su C, Koralov SB, Wang J, Chiu ES, Lu CP.Yu WW, et al.Immunity. 2024 Dec 10;57(12):2827-2842.e5. doi: 10.1016/j.immuni.2024.11.010.Immunity. 2024.PMID: 39662091
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