bioRxiv : the preprint server for biology · 2023
Tertiary Lymphoid Structures Sustain Cutaneous B cell Activity in Hidradenitis Suppurativa.
ПрепринтСтатьяНазвание и аннотация: Перевод пока не подготовлен
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Lowe Margaret M, Cohen Jarish N, Moss Madison I, Clancy Sean, Adler James, Yates Ashley, Naik Haley B, Pauli Mariela, Taylor Ian, McKay Austin, Harris Hobart, Kim Esther, Hansen Scott L, Rosenblum Michael D, Moreau Joshua M
Аннотация
BACKGROUND: Hidradenitis suppurativa (HS) skin lesions are highly inflammatory and characterized by a large immune infiltrate. While B cells and plasma cells comprise a major component of this immune milieu the biology and contribution of these cells in HS pathogenesis is unclear.
OBJECTIVE: We aimed to investigate the dynamics and microenvironmental interactions of B cells within cutaneous HS lesions.
METHODS: We combined histological analysis, single-cell RNA-sequencing (scRNAseq), and spatial transcriptomic profiling of HS lesions to define the tissue microenvironment relative to B cell activity within this disease.
RESULTS: Our findings identify tertiary lymphoid structures (TLS) within HS lesions and describe organized interactions between T cells, B cells, antigen presenting cells and skin stroma. We find evidence that B cells within HS TLS actively undergo maturation, including participation in germinal center reactions and class switch recombination. Moreover, skin stroma and accumulating T cells are primed to support the formation of TLS and facilitate B cell recruitment during HS.
CONCLUSION: Our data definitively demonstrate the presence of TLS in lesional HS skin and point to ongoing cutaneous B cell maturation through class switch recombination and affinity maturation during disease progression in this inflamed non-lymphoid tissue.
OBJECTIVE: We aimed to investigate the dynamics and microenvironmental interactions of B cells within cutaneous HS lesions.
METHODS: We combined histological analysis, single-cell RNA-sequencing (scRNAseq), and spatial transcriptomic profiling of HS lesions to define the tissue microenvironment relative to B cell activity within this disease.
RESULTS: Our findings identify tertiary lymphoid structures (TLS) within HS lesions and describe organized interactions between T cells, B cells, antigen presenting cells and skin stroma. We find evidence that B cells within HS TLS actively undergo maturation, including participation in germinal center reactions and class switch recombination. Moreover, skin stroma and accumulating T cells are primed to support the formation of TLS and facilitate B cell recruitment during HS.
CONCLUSION: Our data definitively demonstrate the presence of TLS in lesional HS skin and point to ongoing cutaneous B cell maturation through class switch recombination and affinity maturation during disease progression in this inflamed non-lymphoid tissue.