Method for constructing heterozygote mouse model with IL-1f9K124A point mutation

The construction of IL-1f9K124A point mutant mice using CRISPR/Cas9 gene editing and imiquimod induction addresses the limitations of existing silver dermatitis models by creating a model with severe skin inflammation and consistent T-cell and neutrophil infiltration, closely mimicking human silver dermatitis and enhancing research applicability.

CN119709877APending Publication Date: 2025-03-28TAIYUAN CENT HOSPITAL
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Patent Information

Application Number
CN202410895708.1
Authority / Receiving Office
CN · China
Patent Type
Applications(China)
Current Assignee / Owner
Filing Date
2024-07-05
Publication Date
2025-03-28

AI Technical Summary

Technical Problem

Current silver dermatitis animal models fail to comprehensively mimic the disease's characteristics, with self-induced models lacking T-cell and neutrophil infiltration, gene-engineered models showing inconsistent skin lesions, and xenotransplant models being costly and prone to immune deficiencies, limiting their applicability and reliability for research and drug development.

Method used

Construction of IL-1f9K124A point mutant mice using CRISPR/Cas9 gene editing to simulate reduced lysine 2-hydroxyisobutyrylation of IL-1F9, combined with imiquimod induction, to create a model that more accurately replicates the skin and inflammatory features of human silver dermatitis.

Benefits of technology

The approach results in a more consistent and severe skin inflammation model that closely resembles human silver dermatitis, with increased T-cell and neutrophil infiltration, reducing the impact of transcriptional and translational variability and shortening the model development time to five days, making it more suitable for research.

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Abstract

The invention relates to a method for constructing a heterozygote mouse model with IL-1f9K124A point mutation. The method comprises the following steps: step 1, acquiring Cas9mRNA (messenger ribonucleic acid), gRNA (guide ribonucleic acid) and oligo donor DNA (deoxyribonucleic acid); step 2, carrying out micro-injection on the Cas9mRNA, the gRNA and the oligo donor DNA obtained in the step 1 into a fertilized egg male pronucleus of a C57BL / 6J mouse, transplanting the fertilized egg after injection into the uterus of a pseudopregnant female mouse, and inoculating the born mouse in such a way as an F0-generation mouse; 3, performing genotype identification on the F0-generation mice through PCR amplification and sequencing, mating the identified F0-generation positive mice with C57BL / 6J mice, and breeding to obtain F1-generation mice; 4, performing genotype identification on the F1-generation mice through PCR amplification and sequencing to obtain F1-generation positive mice which are IL-1f9K124A point mutation heterozygote mice which can be stably inherited; and 5, carrying out imiquimod induction on the heterozygote mouse with IL-1f9K124A point mutation obtained in the step 4 to obtain the psoriasis mouse model. Compared with the prior art, the invention has obvious progress.
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