银屑病疾病模型

疾病简介

银屑病(psoriasis)是一种常见并易复发的慢性炎症性皮肤病,具有特征性红色丘疹、斑块及银白色鳞屑,顽固难治,频繁复发,罹患终身等特点,其发病原因及发病机制均尚未完全明晰,目前认为是遗传和环境因素共同作用导致。

疾病模型

南模生物长期致力于自身免疫性疾病相关研究,开发了多种银屑病小鼠模型,为相关药物的药效评估和安全性评价提供了强有力的工具。

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Fig.1 Body weight (A) and body weight change (B) of IMQ induced Psoriasis model in hIL17A/hIL17F mice. (n=6). 

Test article 1 and test article 2 are from a collaborator.

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Fig.2 IMQ induced Psoriasis model in hIL17A/hIL17F mice. (A) ear thickness (B) skin thickness (C) clinical score (n=6). 

Test article 1 and test article 2 are from a collaborator. Mean ± SEM. t-test, *P < 0.05, **P < 0.01, ***P < 0.001.

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Fig.3 IMQ induced Psoriasis model in hIL17A/hIL17F mice. 

At the study endpoint, back skin samples were harvested and stained with H&E. Representative H&E staining images of the back skin from mice and histological changes were quantified using Baker system.  Results indicated that Bimekizumab significantly reduced skin lesions in IMQ induced Psoriasis model in hIL17A/hIL17F mice (n=6). 

Test article 1 and test article 2 are from a collaborator. Mean ± SEM. t-test, ***P < 0.001.

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Fig.4 IMQ induced Psoriasis model in hIL17A/hIL17F mice. 

At the study endpoint, back skin samples were harvested and hIL17F was tested by qPCR. Results indicated that Bimekizumab significantly reduced hIL17F expression level in IMQ induced Psoriasis model in hIL17A/hIL17F mice(n=6). 

Test article 1 and test article 2 are from a collaborator. Mean ± SEM. t-test, *P < 0.05.

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Fig.1 IMQ induced Psoriasis model in Balb/c. (A) body weight and (B) body weight change. *P<0.05, **P<0.01, ***P<0.001 vs G2.

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Fig.2 IMQ induced Psoriasis model in Balb/c. (A) ear thickness (B) skin thickness (C) cumulative score of PASI. ***P<0.001, *P<0.05 vs G2.

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Fig.3 IMQ induced Psoriasis model in Balb/c. (A) erythema score, (B) skin thickness score and (C) scabby score. ***P<0.001, **P<0.01, *P<0.05 vs G2.

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Fig.4 IMQ induced Psoriasis model in Balb/c. (A) spleen weight, (B) spleen index, (C) spleen image and (D) dorsal image on day3. ***P<0.001 vs G2.

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Fig.5 IMQ induced Psoriasis model in Balb/c. (A) serum TNF-α, (B) serum IL-23 and (C) serum IL-17A. ***P<0.001,  *P<0.05 vs G2.

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Fig.6 IMQ induced Psoriasis model in Balb/c. (A) Tnf-α (B) Il-23 (C) Il-17 mRNA expression of skin. (n=5). ***P<0.001, **P<0.01 vs G2.

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Fig.7 IMQ induced Psoriasis model in Balb/c. (A) Pathological Score (B) Epidermis thickness (C) typical pathology image. ****P<0.001, **P<0.01 vs G2.

Case 1

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Fig.1 IMQ induced Psoriasis model based on hIL23A mice.


Case 2

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Fig 2. The efficacy of Guselkumab in an IMQ-induced psoriasis model in hIL23 mice. (A) Body weight and (B) body weight change over the study duration.

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Fig 3. Skin thickening measurements in an IMQ-induced psoriasis model in hIL23 mice. (A) Ear thickness and (B) dorsal skin thickness.

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Fig 4. Clinical scoring in an IMQ-induced psoriasis model in hIL23 mice. (A) Total clinical score, composed of (B) erythema, (C) skin thickness, and (D) scabbing scores.

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Fig 5. Histological evaluation in an IMQ-induced psoriasis model in hIL23 mice. (A) Representative photographs of H&E-stained ear sections. (B) Pathological score. (C) Epidermis thickness.

  • Rat IL23-induced Psoriasis model in SD Rat

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Fig.1 rIL23-induced Psoriasis model in SD Rat. (A) Body weight. (B) Body weight change.

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Fig.2 rIL23-induced Psoriasis model in SD Rat. (A) Ear thickness. (B) Ear thickness change. (C) PASI score.

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Fig.3 Representative photo of rIL23-induced Psoriasis model in SD Rat. 

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Fig.4 rIL23-induced Psoriasis model in SD Rat. (A) Representative photo of H&E staining. (B) Baker score. 


  • Human IL23-induced Psoriasis model in SD Rat

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Fig.1 hIL23-induced Psoriasis model in SD Rat. (A) Body weight. (B) Body weight change.

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Fig.2 hIL23-induced Psoriasis model in SD Rat. (A) Ear thickness. (B) Ear thickness change. (C) PASI score.

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Fig.3 Representative photo of hIL23-induced Psoriasis model in SD Rat.

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Fig.4 hIL23-induced Psoriasis model in SD Rat. (A) Representative photo of H&E staining. (B) Baker score. 

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Fig.1 Body weight and body weight change among time during study. Body weight and body weight change in anti-IL23 treated imiquimod (IMQ)-induced psoriasis in HO hTL1A/hIL23A/hIL12B mice (n=3-4 /group, 6weeks, male). IMQ treatment induced body weight loss in male hTL1A/hIL23A/hIL12B mice. Risankizumab treatment didn’t alleviate the weight loss.

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Fig.2 Psoriasis evaluation among time during study. In vivo efficacy evaluation of anti-IL23 in imiquimod (IMQ)-induced psoriasis in HO hTL1A/hIL23A/hIL12B mice (n=3-4 /group, 6weeks, male). IMQ treatment successfully induced psoriasis-like skin inflammation in female hTL1A/hIL23A/hIL12B mice, characterized by increased elevated PASI scores (including erythema and scaling) over the 7-day observation period. Notably, Risankizumab alleviated IMQ-induced psoriasis.

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Fig.3 H&E staining of psoriatic skin lesions in IMQ-induced mice. Representative H&E staining images of skin from the (A) control, (B) IMQ+vehicle, and (C) IMQ+Risankizumab groups. Scale bar=500 µm. (D) Baker score based on HE pathology images (n=3/group, 6 weeks old). 

IMQ treatment induced significant psoriasis-like skin thickening and histopathological features, including parakeratosis, spongiosis, dilated capillaries, and lymphocytic infiltration, as observed in the IMQ-treated groups. Risankizumab treatment slightly alleviated these psoriatic symptoms and reduced epidermal thickness, demonstrating its therapeutic effect in this IMQ-induced psoriasis model.

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Fig1. In vivo efficacy evaluation of anti-IL23 and anti-IL23/IL12 in imiquimod (IMQ)-induced psoriasis model in hIL23A/hIL12B mice (3-6 mice/group, 6 weeks, female). 

IMQ treatment induced body weight loss in female hIL-23A/hIL-12B mice. Neither Risankizumab nor Ustekinumab treatment alleviated this weight loss, with both antibody-treated groups showing final body weight reductions.

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Fig2. In vivo efficacy evaluation of anti-IL23 and anti-IL23/IL12 in imiquimod (IMQ)-induced psoriasis model in hIL23A/hIL12B mice (3-6 mice/group, 6 weeks, female).

IMQ treatment successfully induced psoriasis-like skin inflammation in female hIL-23A/hIL-12B mice, characterized by increased skin thickness and elevated PASI scores (including erythema and scaling) over the 7-day observation period. Notably, Risankizumab demonstrated better therapeutic effect than Ustekinumab in lleviating IMQ-induced psoriasis.

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Fig3.H&E staining of psoriatic skin lesions in IMQ-induced mice. Compared to the control group (A) , all IMQ-treated groups displayed skin thickening. The IMQ+Vehicle (B) and IMQ+Ustekinumab (D) groups showed progressive and plaque-stage psoriasis symptoms focal parakeratosis, spongiosis, twisted and dilated capillaries (Black), and lymphocytic infiltration in the dermal papillae (Red), whereas the IMQ+Risankizumab group (C) showed reduced epidermal thickness and ameliorated histopathological features. Scale bar = [500] µm.

IMQ treatment induced significant psoriasis-like skin thickening and histopathological features, including parakeratosis, spongiosis, dilated capillaries, and lymphocytic infiltration, as seen in the IMQ induced groups. Comparing to Ustekinumab, Risankizumab treatment significantly alleviated these psoriatic symptoms and reduced epidermal thickness, demonstrating its therapeutic effect in this IMQ-induced psoriasis model.

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Fig 1. Body weight monitoring in hPD-1/hPD-L1 mice during IMQ challenge. (A) Absolute body weight and (B) body weight change.

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Fig 2. Macroscopic presentation of psoriasis-like lesions. Representative photographs of dorsal skin lesions in hPD-1/hPD-L1 mice taken at the study endpoint.

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Fig 3. Clinical scoring of IMQ-induced lesions. Psoriasis severity was graded based on (A) erythema, (B) scabbing, and (C) cumulative clinical score.

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Fig 4. Quantification of skin thickening. (A) Dorsal skin thickness measurements and (B) skin thickness scoring were performed to evaluate the severity of edema and hyperplasia.

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Fig 5. Assessment of systemic inflammation via spleen indices. (A) Spleen weight and (B) spleen index (spleen weight normalized to body weight) were measured at the endpoint as markers of systemic immune activation.

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Fig 6. Histological evaluation of skin pathology. (A) Representative H&E-stained cross-sections of dorsal skin. (B) Pathological severity was quantified using the Baker score.

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Fig1. The psoriasis model induced by hIL-23 and hTL1A in C57BL/6 mice. (A) Ear thickness. (B) Changes in ear thickness. (C) PASI score. (D) Representative micrographs. (E) Representative H&E-stained micrographs. (F) Baker score.

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