Zvast Biotechnology
Psoriasis
rIL-23 Induced
The rIL-23 induced C57 mouse psoriasis model is a SCI standardized immune-driven gold-standard psoriasis model established by intradermal fixed-point injection of recombinant interleukin-23 (rIL-23), which targets and activates the core IL-23/Th17 inflammatory axis. Different from IMQ-, hormone- and drug-induced models, it specifically simulates the pathogenesis of psoriasis vulgaris driven by upstream IL-23, and accurately recapitulates cutaneous immune disorder, abnormal keratinocyte proliferation and epidermal keratinization lesions triggered by excessive clinical IL-23 secretion.
Recombinant interleukin-23 (rIL-23) is the upstream master pro-inflammatory cytokine of psoriasis. Continuous local intradermal administration directly acts on cutaneous dendritic cells, innate lymphoid cells and CD4⁺ T cells, specifically driving the polarization of naive T cells into Th17 cells and massive secretion of downstream effector cytokines IL-17A, IL-17F and IL-22. These inflammatory factors synergistically stimulate unlimited proliferation of keratinocytes, inhibit normal epidermal differentiation, disrupt skin barrier structure, induce dermal microvascular dilation, and recruit infiltration of neutrophils, macrophages and lymphocytes, and gradually form typical psoriatic lesions including erythema, silvery scaling, epidermal hypertrophy and acanthosis.
C57BL/6 mice are inbred homozygous strains with unified genetic background and uniform immune response, highly sensitive to exogenous rIL-23 stimulation, synchronous lesion progression and minimal individual differences without spontaneous cutaneous inflammation interference. The pathological features fully recapitulate core lesions of human psoriasis: hyperkeratosis, parakeratosis, acanthosis, elongated epidermal rete ridges and superficial dermal inflammatory infiltration, without severe suppurative damage except Munro microabscesses. It serves as an exclusive standard model for elucidating IL-23/Th17 axis mechanisms and evaluating pharmacodynamic effects of IL-23/IL-17 targeted biologics and small-molecule immune regulators, and is widely applied in basic mechanism and translational medical research of autoimmune skin diseases.
Four evaluation dimensions including erythema, scaling, skin thickening and epidermal infiltration were set, each item scored from 0 to 4 points with total score ranging from 0 to 16 points. Score 0 represents completely normal skin, score 4 represents severe single symptom. After modeling, mice in model group presented typical IL-23-induced psoriasiform signs at injection area: persistent erythema with clear boundary, thin silvery scaling, epidermal hypertrophic protuberance and dermal infiltrative edema. The total lesion score was extremely significantly higher than blank control group with statistically significant inter-group differences, confirming preliminary successful model construction.
High-precision digital vernier caliper was used to detect skin thickness at fixed central lesion sites under unified measurement pressure and angle. The skin thickness of model group was significantly higher than blank group, showing IL-17-mediated abnormal epidermal proliferative thickening and dermal inflammatory edema, which fully matches the core epidermal hypertrophy phenotype of psoriasis triggered by IL-23/Th17 pathway activation, serving as an objective quantitative modeling standard.
HE staining of lesional skin showed characteristic pathological changes of IL-23-induced psoriasis: epidermal hyperkeratosis, focal parakeratosis and a small number of Munro microabscesses in stratum corneum; obvious acanthosis and uniformly elongated epidermal rete ridges; vasodilation and congestion in superficial dermis with diffuse infiltration of abundant CD4⁺ T cells, neutrophils and dendritic cells, without severe subcutaneous tissue necrosis. The pathological morphology is highly consistent with mild to moderate clinical psoriasis vulgaris with high IL-23 expression, with strong pathological phenotype specificity.
The expression levels of upstream pro-inflammatory factor IL-23 and downstream Th17 effector factors IL-17A, IL-17F, IL-22 in skin tissues and serum of model group were significantly upregulated with synchronous elevation of TNF-α, presenting specific excessive activation of Th17 immune pathway and obvious imbalance characteristics of IL-23/IL-17 inflammatory axis, which serves as the core academic criterion for confirming successful construction of rIL-23 psoriasis model.
As an exclusive SCI gold-standard psoriasis model targeting IL-23/Th17 pathway, it adopts single stimulant recombinant IL-23 without mixed interference of TLR7/8, hormones and drugs with pure mechanism, and accurately corresponds to clinical autoimmune psoriasis induced by overexpressed IL-23. Inbred C57 mice with consistent genetic background possess far higher experimental reproducibility than outbred KM mice and SD rats. It features 7-day short-term modeling, minimally invasive operation, zero animal mortality and mild controllable lesions. It is specially applied to pharmacodynamic screening of immune targeted drugs such as IL-23 receptor antagonists, anti-IL-17 monoclonal antibodies and Th17 differentiation inhibitors. The project has clear mechanism targets and prominent innovation with highly recognized data for high-score SCI journals, suitable for psoriasis immune mechanism projects, preclinical evaluation of biological agents, master and doctoral dissertations and fund declaration.
The rIL-23 induced C57 mouse psoriasis model is corely applied to basic research on autoimmune regulation mechanism of IL-23/Th17 inflammatory axis, IL-17-mediated keratinocyte proliferation pathway and dendritic cell pro-inflammatory activation mechanism. It is specially used to evaluate targeted pharmacodynamic effects of various immune preparations, small-molecule inhibitors and active ingredients of traditional Chinese medicines on blocking IL-23 secretion, inhibiting Th17 differentiation, downregulating IL-17 family factors, repairing skin barrier and alleviating erythema and scaling lesions. It is widely suitable for immune target exploration of autoimmune skin diseases, preclinical screening of anti-psoriatic biological drugs and translational research of immunomodulatory natural products, serving as an irreplaceable standardized special model for psoriasis immune mechanism research.
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