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Related Experiment Video

Updated: Jun 29, 2026

Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes

Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes

Published on: September 27, 2013

Organ-specific disease provoked by systemic autoimmunity

V Kouskoff¹, A S Korganow, V Duchatelle

¹Institut de Génétique et de Biologie Moléculaire et Cellulaire (CNRS/INSERM/ULP), Illkirch, France.

|November 29, 1996

Summary

Researchers developed a mouse model for rheumatoid arthritis (RA) by crossing specific mouse strains. This model mimics human RA, offering new insights into the autoimmune disease and its potential triggers.

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Last Updated: Jun 29, 2026

Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes

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Published on: September 27, 2013

Development of Stem Cell-derived Antigen-specific Regulatory T Cells Against Autoimmunity

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Published on: November 8, 2016

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

Published on: March 17, 2023

Area of Science:

Immunology
Autoimmunity
Rheumatology

Background:

Rheumatoid arthritis (RA) is a chronic joint disease with poorly understood causes.
RA involves leukocyte invasion, synoviocyte activation, and subsequent cartilage/bone destruction.

Purpose of the Study:

To describe a novel spontaneous mouse model that mimics human rheumatoid arthritis.
To investigate the underlying mechanisms of joint disease development in this model.

Main Methods:

Generation of a mouse model by crossing a T cell receptor (TCR) transgenic line with the NOD strain.
Observation of disease development in offspring, characterized as a joint disease reminiscent of human RA.

Main Results:

All offspring developed a joint disease similar to human RA.
The trigger involved recognition of a NOD-derived major histocompatibility complex (MHC) class II molecule by the transgenic TCR.
Arthritis progression involved CD4+ T cells, B cells, and myeloid cells.

Conclusions:

Joint-specific diseases can arise from a breakdown in self-tolerance, leading to systemic self-reactivity.
This mouse model provides a valuable tool for studying RA pathogenesis.
Human RA may develop through a similar mechanism involving systemic autoimmunity.