Galectin-1 deficiency attenuates imiquimod-induced psoriasiform skin inflammation and is associated with reduced macrophage recruitment
7 affiliations
- 1Department of Microbiology and Immunology, National Cheng Kung University Medical College , ,
- 2Department of Nursing, College of Nursing, Chung Hwa University of Medical Technology , ,
- 3Department of Pediatrics, Ditmanson Medical Foundation Chia-Yi Christian Hospital , ,
- 4Department of Medical Research, Ditmanson Medical Foundation Chia-Yi Christian Hospital , ,
- 5Department of Internal Medicine, National Cheng Kung University Medical College , ,
- 6Institute of Oral Medicine, National Cheng Kung University Medical College , ,
- 7Department of Biochemistry and Molecular Biology, National Cheng Kung University Medical College , ,
Abstract
Introduction: Psoriasis is an immune-mediated inflammatory skin disease in which innate immune activation and the IL-23/IL-17 axis coordinate keratinocyte hyperproliferation and leukocyte recruitment. Galectin-1 (Gal-1) is a glycanbinding protein with context-dependent immunoregulatory effects; however, its function in psoriasiform skin inflammation remains incompletely defined. Methods: Here, we evaluated Gal-1 expression in human psoriasis lesions and investigated its contribution to imiquimod (IMQ)-induced psoriasiform inflammation in mice.
Results: Gal-1 immunoreactivity was increased in lesional skin from patients with psoriasis and in IMQ-treated wildtype mice. Compared with IMQ-treated wild-type mice, Gal-1-deficient mice developed less severe erythema, scaling, epidermal thickening, acanthosis, and parakeratosis. Attenuated disease was accompanied by reduced lymphoidorgan enlargement and lower frequencies or numbers of selected innate and adaptive immune-cell populations. In skin, Gal-1 deficiency was associated with reduced macrophage accumulation and diminished CXCL10 mRNA expression, whereas several other inflammatory transcripts showed variable, non-significant trends. In vitro, macrophages from Gal-1 deficient mice displayed impaired migration, while recombinant Gal-1 enhanced macrophage migration in cells from both genotypes.
Conclusion: These findings support Gal-1 as a potential therapeutic target for modulating inflammatory-cell recruitment and alleviating psoriasiform skin inflammation.
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BibTeX
@article{yang2026galectin1,
title = {{Galectin-1 deficiency attenuates imiquimod-induced psoriasiform skin inflammation and is associated with reduced macrophage recruitment}},
author = {Shiu-Ju Yang and Shih-Yao Chen and Chia-Hsin Hou and Chao-Liang Wu and Ming-Fei Liu and Yuh-Ling Chen and Tak-Wah Wong and Chuang-Ming Wang and Ai-Li Shiau},
journal = {Frontiers in immunology},
year = {2026},
month = sep,
doi = {10.3389/fimmu.2026.1960116},
url = {https://europepmc.org/article/PMC/PMC13661995},
note = {CC BY},
}
RIS
TY - JOUR
TI - Galectin-1 deficiency attenuates imiquimod-induced psoriasiform skin inflammation and is associated with reduced macrophage recruitment
AU - Shiu-Ju Yang
AU - Shih-Yao Chen
AU - Chia-Hsin Hou
AU - Chao-Liang Wu
AU - Ming-Fei Liu
AU - Yuh-Ling Chen
AU - Tak-Wah Wong
AU - Chuang-Ming Wang
AU - Ai-Li Shiau
PY - 2026
DA - 2026/09/30
JO - Frontiers in immunology
DO - 10.3389/fimmu.2026.1960116
UR - https://europepmc.org/article/PMC/PMC13661995
AB - Introduction: Psoriasis is an immune-mediated inflammatory skin disease in which innate immune activation and the IL-23/IL-17 axis coordinate keratinocyte hyperproliferation and leukocyte recruitment. Galectin-1 (Gal-1) is a glycanbinding protein with context-dependent immunoregulatory effects; however, its function in psoriasiform skin inflammation remains incompletely defined. Methods: Here, we evaluated Gal-1 expression in human psoriasis lesions and investigated its contribution to imiquimod (IMQ)-induced psoriasiform inflammation in mice. Results: Gal-1 immunoreactivity was increased in lesional skin from patients with psoriasis and in IMQ-treated wildtype mice. Compared with IMQ-treated wild-type mice, Gal-1-deficient mice developed less severe erythema, scaling, epidermal thickening, acanthosis, and parakeratosis. Attenuated disease was accompanied by reduced lymphoidorgan enlargement and lower frequencies or numbers of selected innate and adaptive immune-cell populations. In skin, Gal-1 deficiency was associated with reduced macrophage accumulation and diminished CXCL10 mRNA expression, whereas several other inflammatory transcripts showed variable, non-significant trends. In vitro, macrophages from Gal-1 deficient mice displayed impaired migration, while recombinant Gal-1 enhanced macrophage migration in cells from both genotypes. Conclusion: These findings support Gal-1 as a potential therapeutic target for modulating inflammatory-cell recruitment and alleviating psoriasiform skin inflammation.
SN - 1664-3224
ER -