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TIGIT agonism as a therapeutic strategy to suppress inflammation in hidradenitis suppurativa
Journal article   Open access   Peer reviewed

TIGIT agonism as a therapeutic strategy to suppress inflammation in hidradenitis suppurativa

Michal Kidacki, Anjali Jaiswal, Christina Cho, Samantha Prince, Rachel Breidbart, Henry Hsia, Matthew D. Vesely and Lieping Chen
Frontiers in immunology, Vol.17, 1761782
04/01/2026
DOI: 10.3389/fimmu.2026.1761782
PMID: 41993172
url
https://doi.org/10.3389/fimmu.2026.1761782View
Published (Version of record) Open Access

Abstract

Hidradenitis suppurativa (HS) is a chronic, heterogeneous inflammatory skin disorder with limited therapeutic options. The immune checkpoint receptor TIGIT is emerging as a regulator of chronic inflammation, yet its role in HS remains unknown. Here, we investigated TIGIT and its ligands in HS using tissue profiling, transcriptomics, and an ex vivo functional explant model. A tissue microarray containing 52 HS, 9 ruptured follicular cysts, and 4 normal skin samples demonstrated significantly increased TIGIT expression in HS lesions. In contrast, the TIGIT ligand PVRL3 was significantly decreased in HS, a finding also observed in a publicly available RNA-seq dataset. Because TIGIT suppresses inflammation only when adequately engaged by its ligands, reduced PVRL3 may impair inhibitory checkpoint signaling in HS. To test whether TIGIT engagement could suppress HS inflammation, we developed an ex vivo explant model using freshly obtained HS lesional tissue. The system was validated using triamcinolone, a corticosteroid, which consistently reduced IL-6 production. Treatment with a TIGIT agonist antibody significantly reduced IL-6 by 72 hours. These findings provide the first functional evidence that TIGIT activation attenuates inflammatory pathways in HS, supporting TIGIT agonism as a potential therapeutic strategy.
 Inflammation hidradenitis suppurativa immune checkpoint PVRL3 TIGIT

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