Frontiers in immunology · 2026
Peripheral γδ T-cell remodeling in psoriasis is associated with effector-biased transcriptional organization and reduced representation of a circulating CSMD1-marked state.
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Shi Nanxi, Chen Yiming, Tang Jiale, Chen Sihan, Lin Xi, Ye Yingying, Zhang Jingsong, Chen Ruili, Zeng Jiaqi, Sun Guodong, Yang Xiaoqiao, Zhong Suhua, Huang Fang, Li Zhenhua, Tang Xin, Wu Shi, Liang Yunting
Аннотация
BACKGROUND: Despite the prominent immune dysregulation in psoriasis, the organization of peripheral blood γδ T cell states remains incompletely defined.
METHODS: Here, we performed single-cell transcriptomic profiling of enriched peripheral blood-derived γδ T cells from healthy donors and patients with psoriasis. By integrating state annotation, inferred transcriptional ordering, ligand-receptor communication, transcriptome-inferred metabolite-sensor communication, and regulatory network analyses, we constructed a circulating γδ T-cell state atlas.
RESULTS: We identified eight γδ T-cell states. Within the resolution of this dataset, psoriasis-derived cells did not form a clearly separated disease-exclusive state; instead, disease-associated changes were mainly reflected by altered representation and transcriptional organization of pre-existing states, including reduced peripheral representation of a CSMD1-marked γδ T-cell state. Pseudotime analysis arranged γδ T cells along an inferred activation- and cytotoxicity-associated transcriptional continuum, with Naive-like cells at the lower-pseudotime region and cytotoxic effector-, NK-like-, cytotoxic memory-like-, terminal-branch-, and CSMD1-marked states toward higher-pseudotime regions. Psoriasis-derived γδ T cells were more frequent in cytotoxicity-related regions. This pattern suggests a shift toward effector states. In parallel, peripheral γδ T cell communication suggested cytotoxic-state-biased ligand-receptor patterns, with rewiring of MIF-related and metabolic signaling and reduced network participation of CSMD1 + γδ T cells. Regulatory analyses further linked FOXP1, STAT1, and NFATC3 as candidate regulators associated with early-like, transitional/CSMD1-marked, and cytotoxic-associated transcriptional states, respectively.
CONCLUSIONS: These findings support a state-resolved framework of circulating γδ T-cell remodeling in psoriasis and identify reduction and possible redistribution of a CSMD1-marked late-stage state as a feature of disease-associated immune remodeling.
METHODS: Here, we performed single-cell transcriptomic profiling of enriched peripheral blood-derived γδ T cells from healthy donors and patients with psoriasis. By integrating state annotation, inferred transcriptional ordering, ligand-receptor communication, transcriptome-inferred metabolite-sensor communication, and regulatory network analyses, we constructed a circulating γδ T-cell state atlas.
RESULTS: We identified eight γδ T-cell states. Within the resolution of this dataset, psoriasis-derived cells did not form a clearly separated disease-exclusive state; instead, disease-associated changes were mainly reflected by altered representation and transcriptional organization of pre-existing states, including reduced peripheral representation of a CSMD1-marked γδ T-cell state. Pseudotime analysis arranged γδ T cells along an inferred activation- and cytotoxicity-associated transcriptional continuum, with Naive-like cells at the lower-pseudotime region and cytotoxic effector-, NK-like-, cytotoxic memory-like-, terminal-branch-, and CSMD1-marked states toward higher-pseudotime regions. Psoriasis-derived γδ T cells were more frequent in cytotoxicity-related regions. This pattern suggests a shift toward effector states. In parallel, peripheral γδ T cell communication suggested cytotoxic-state-biased ligand-receptor patterns, with rewiring of MIF-related and metabolic signaling and reduced network participation of CSMD1 + γδ T cells. Regulatory analyses further linked FOXP1, STAT1, and NFATC3 as candidate regulators associated with early-like, transitional/CSMD1-marked, and cytotoxic-associated transcriptional states, respectively.
CONCLUSIONS: These findings support a state-resolved framework of circulating γδ T-cell remodeling in psoriasis and identify reduction and possible redistribution of a CSMD1-marked late-stage state as a feature of disease-associated immune remodeling.