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Mouse Models for Graft Arteriosclerosis

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A humanized HLA-DR4 mouse model for autoimmune myocarditis.

M Emrah Şelli¹, Anita C Thomas¹, David C Wraith²

¹University of Bristol, School of Clinical Sciences, UK; Bristol Heart Institute, Bristol Royal Infirmary, Bristol BS2 8HW, UK.

Journal of Molecular and Cellular Cardiology

|April 23, 2017

Summary

A new mouse model mimics human autoimmune myocarditis, a cause of heart failure. Treatment with specific peptides improved cardiac function, offering potential for new therapies targeting autoimmune heart disease.

Keywords:

Autoimmunity Cardiomyopathy Heart failure Myocarditis

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Production of Humanized Mouse via Thymic Renal Capsule Grafting, CD34+ Cells Injection, and Cytokine Delivery

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Published on: September 27, 2021

Area of Science:

Immunology
Cardiology
Genetics

Background:

Myocarditis, a leading cause of heart failure in young adults, is linked to autoimmunity against human cardiac α-myosin (hCAM) and the human major histocompatibility II (MHCII) DR4 allele.
Understanding the mechanisms of hCAM-induced myocarditis is crucial for developing effective treatments.

Purpose of the Study:

To develop a humanized mouse model for studying hCAM-induced autoimmune myocarditis.
To evaluate the therapeutic potential of hCAM-derived peptides in this model.

Main Methods:

Development of a mouse model using human HLA-DR4 transgenic mice lacking mouse MHCII genes, immunized with hCAM.
Assessment of immune responses (T-cell proliferation, antibody titers), cardiac function (echocardiography), and cardiac histology.
Treatment of the model with hCAM-derived peptides.

Main Results:

Immunization induced splenic T-cell proliferation, increased antibody titers, cardiac inflammation, and impaired cardiac function (reduced cardiac output and fractional shortening).
Treatment with hCAM-derived peptides significantly preserved ejection fraction and fractional shortening.
Prolonging the experiment led to mortality, but cardiac dilatation and fibrosis were not observed at the initial time point.

Conclusions:

The developed humanized mouse model effectively replicates key features of hCAM-induced autoimmune myocarditis.
hCAM-derived peptides show therapeutic promise for preserving cardiac function in autoimmune cardiomyopathy.
This model serves as a valuable platform for refining peptide-based treatments for autoimmune heart conditions.