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Background <p>Psoriasis is a chronic inflammatory disease characterized by keratinocyte hyperproliferation, immune cell infiltration, and persistent inflammatory signaling. Although Tm4sf19 has been implicated in inflammatory processes, its contribution to psoriasis pathogenesis remains unclear.</p> Methods <p>We investigate the role of Tm4sf19 in psoriatic inflammation was examined using an imiquimod-induced psoriasis mouse model and HaCaT keratinocytes, in which Tm4sf19 expression was deleted genetically or suppressed pharmacologically with the competitive inhibitor, LEL-Fc. Gene expression, protein expression, and tissue changes were assessed by qPCR, western blotting and histological scoring, respectively.</p> Results <p>Tm4sf19 expression was significantly elevated in psoriatic lesion. Tm4sf19 knockout or inhibition using LEL-Fc suppressed psoriatic symptoms, macrophage-mediated inflammation and inflammatory cytokine expression. Tm4sf19 inhibition also suppressed the activation of STAT3, EGFR, ERK and KRT17 signaling pathways in keratinocytes. Furthermore, LEL-Fc treatment effectively inhibited LPS-induced cell cycle progression and promoted apoptosis in keratinocyte both in vivo and in vitro.</p> Conclusion <p>These findings suggest that Tm4sf19 regulates psoriatic inflammation and keratinocyte proliferation through major signaling pathways. Therefore, inhibiting Tm4sf19 may have therapeutic potential for the treatment of psoriasis.</p>

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Tm4sf19 inhibition alleviates imiquimod-induced psoriatic dermatitis by regulating inflammatory signaling pathways and keratinocyte proliferation in mice

  • 期刊论文

  • 发表日期：

    2026年4月17日

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  • Min Gi Kang,
  • Sujin Park,
  • Eunji Hong,
  • Min-Jung Lee,
  • Da Seul Jung,
  • Jin Sun Heo,
  • Haein An,
  • Min Woo Kim,
  • Naim Park,
  • Hyeyeon Park,
  • Pyunggang Kim,
  • Minjung Son,
  • Kyoungwha Pang,
  • Jinah Park,
  • Ga-Eun Hwang,
  • Yong Jung Kwon,
  • Seiya Mizuno,
  • Satoru Takahashi,
  • Seok Hee Park,
  • Seong-Jin Kim

摘要

Background

Psoriasis is a chronic inflammatory disease characterized by keratinocyte hyperproliferation, immune cell infiltration, and persistent inflammatory signaling. Although Tm4sf19 has been implicated in inflammatory processes, its contribution to psoriasis pathogenesis remains unclear.

Methods

We investigate the role of Tm4sf19 in psoriatic inflammation was examined using an imiquimod-induced psoriasis mouse model and HaCaT keratinocytes, in which Tm4sf19 expression was deleted genetically or suppressed pharmacologically with the competitive inhibitor, LEL-Fc. Gene expression, protein expression, and tissue changes were assessed by qPCR, western blotting and histological scoring, respectively.

Results

Tm4sf19 expression was significantly elevated in psoriatic lesion. Tm4sf19 knockout or inhibition using LEL-Fc suppressed psoriatic symptoms, macrophage-mediated inflammation and inflammatory cytokine expression. Tm4sf19 inhibition also suppressed the activation of STAT3, EGFR, ERK and KRT17 signaling pathways in keratinocytes. Furthermore, LEL-Fc treatment effectively inhibited LPS-induced cell cycle progression and promoted apoptosis in keratinocyte both in vivo and in vitro.

Conclusion

These findings suggest that Tm4sf19 regulates psoriatic inflammation and keratinocyte proliferation through major signaling pathways. Therefore, inhibiting Tm4sf19 may have therapeutic potential for the treatment of psoriasis.