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CD147 Is Essential for the Development of Psoriasis via the Induction of Th17 Cell Differentiation.

ABSTRACT: Th17 cells play an important role in psoriasis. The differentiation of naïve CD4⁺ T cells into Th17 cells depends on glycolysis as the energy source. CD147/basigin, an integral transmembrane protein belonging to the immunoglobulin superfamily, regulates glycolysis in association with monocarboxylate transporters (MCTs)-1 and -4 in cancer cells and T cells. We examined whether CD147/basigin is involved in the pathogenesis of psoriasis in humans and psoriasis-model mice. The serum level of CD147 was increased in patients with psoriasis, and the expression of CD147 and MCT-1 was elevated in their dermal CD4⁺ RORγt⁺ T cells. In vitro, the potential of naïve CD4⁺ T cells to differentiate into Th17 cells was abrogated in CD147^-/- T cells. Imiquimod (IMQ)-induced psoriatic dermatitis was significantly milder in CD147^-/- mice and bone marrow chimeric mice lacking CD147 in the hematopoietic cells of myeloid lineage. These findings demonstrate that CD147 is essential for the development of psoriasis via the induction of Th17 cell differentiation.

SUBMITTER: Okubo A

PROVIDER: S-EPMC8745261 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:BackgroundPsoriasis is a chronic autoimmune disease. At present, it is very difficult to treat; however, clinical trials have shown that the traditional Chinese medicine (TCM) treatment of psoriasis has certain advantages. The Chinese herbal medicine Jia Wei Jing Xie Yin (JWJXY) has its origins in Jing Xie Yin, a medicine created by the TCM doctor Wu Jun. Previous studies have shown that JWJXY has good clinical efficacy for patients with blood-heat type psoriasis, but its mechanism is unknown.MethodsThis paper aimed to further study the therapeutic effect and mechanism of JWJXY on an imiquimod (IMQ)-induced, psoriasis-like mouse model (0.4 mL, i.g., 6 days). The histopathological skin changes were observed by hematoxylin and eosin (HE) staining, the infiltration of cluster of differentiation 11B (CD11b) and cluster of differentiation 4 (CD4) cells was observed by immunohistochemistry, lymphocyte subsets were detected by flow cytometry, T helper (Th)17 cell expression was perceived by flow cytometry, and Th17 cell-related gene expression was detected by real-time quantitative polymerase chain reaction (qPCR).ResultsJWJXY significantly reduced the skin thickness of the IMQ-induced model mouse. Compared with that in the vehicle group, the skin tissue of the mice in the JWJXY group showed significantly reduced infiltration of CD11b+ and CD4+ T cells. Flow cytometry results showed that JWJXY decreased the proportion of B220 and Th17 cells in the spleen tissue of the mice. There was no significant effect on the proportion of Th1 or regulatory T cells (Treg) cells. Compared with that in the vehicle group, the skin tissue of the mice in the JWJXY group showed significantly decreased expression of interleukin-17A (IL-17A), IL-17F, retinoic acid receptor-related orphan receptor gamma t (RORγt), IL-1β, interferon gamma (IFN-γ), and tumor necrosis factor alpha (TNF-α) messenger RNA (mRNA).ConclusionsThe study confirmed the therapeutic effect of JWJXY on psoriasis. Its mechanism of action might be to inhibit the Th17 cell response but not the Th1 and Treg response.

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CD147 Is Essential for the Development of Psoriasis via the Induction of Th17 Cell Differentiation.

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