• Modeling Mechanism：

  Imiquimod hydrochloride, as a TLR7 agonist, activates skin keratinocytes and immune cells, induces IL-23/IL-17 axis activation, promotes the release of pro-inflammatory factors such as CXCL1 and IL-6, and recruits neutrophils to infiltrate; it causes abnormal proliferation of keratinocytes and epidermal thickening, while damaging the skin barrier function, leading to desquamation and plaque formation.

• Related Products：

  Imiquimod hydrochloride (T22091)

• Modeling Method：

  Experimental Subject：

  Mice, C57BL/6N background (K5-ILFO transgenic mice and ILFO control mice), 8-12 weeks old, Shave dorsal skin hair 1 day prior to modelling

  Dosage and Administration Route：

  62.5 mg 5% Imiquimod cream , applied evenly to dorsal skin

  Dosing Frequency and Duration Model：

  Once daily for 3–7 consecutive days

• Validation：

  The Psoriasis Area and Severity Index (PASI) was elevated, manifested as skin erythema, thickening, and desquamation; the epidermis was significantly thickened, and the arrangement of keratinocytes was disordered; the mRNA and protein levels of Krt6, Krt16 (keratinocyte activation marker), IL-6, CXCL1, IL-17A, and Ly6g (neutrophil marker) in the skin tissue were significantly elevated.

*Precautions： Mice were sacrificed 3 or 7 days after modeling, and back skin and plasma samples were quickly separated. Some skin tissue was fixed in formalin (for histological examination), and some was cryopreserved for protein and RNA extraction.

*References：Huard A, et,al. Interleukin-38 overexpression in keratinocytes limits desquamation but does not affect the global severity of imiquimod-induced skin inflammation in mice. Front Immunol. 2024 Jul 25;15:1387921.