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GPR108 Negatively Regulates TLR7 Signaling in Imiquimod-Induced Psoriasiform Dermatitis
Wenwen Wang1,2, Yuyan Zhang3, Kainan Liao1
1Department of Biochemistry and Molecular Biology, Anhui Medical University, Hefei, China.
Immunity, Inflammation and Disease
|February 13, 2026
Summary
G protein-coupled receptor 108 (GPR108) negatively regulates Toll-like receptor 7 (TLR7) signaling. GPR108 deficiency exacerbates imiquimod-induced psoriasis-like skin inflammation by enhancing TLR7 activation.
Area of Science:
- Dermatology
- Immunology
- Molecular Biology
Background:
- Psoriasis is a chronic inflammatory skin disease driven by endosomal Toll-like receptors (TLRs), especially TLR7.
- Mechanisms regulating TLR7 activity in psoriasis are not fully understood.
Purpose of the Study:
- Investigate the role of G protein-coupled receptor 108 (GPR108) in regulating TLR7 activity.
- Examine GPR108's function in imiquimod (IMQ)-induced psoriasiform dermatitis.
Main Methods:
- Utilized Gpr108-null mice and GPR108-deficient keratinocyte/macrophage models with IMQ-induced lesions.
- Assessed phenotype via PASI scoring, H&E staining, Western blotting, IHC, IF, RNA-seq, and flow cytometry.
- Verified TLR7/NF-κB signaling involvement in macrophage polarization.
Main Results:
- Gpr108 deficiency worsened IMQ-induced psoriatic lesions.
- GPR108 deficiency enhanced TLR7/MyD88/NF-κB signaling in keratinocytes and macrophages.
- This led to increased keratinocyte proliferation, altered macrophage balance, and elevated TNF-α and IL-6 production.
Conclusions:
- GPR108 acts as a negative regulator of TLR7 signaling in psoriasis.
- Targeting GPR108 may offer a novel therapeutic strategy for psoriasis.
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