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Autoimmune arthritis: Transgenic mouse models and methods.

Lauren M F Merlo1, Weidan Peng1, Laura Mandik-Nayak1

  • 1Lankenau Institute for Medical Research, Wynnewood, PA, United States.

Methods in Cell Biology
|October 17, 2025
PubMed
Summary
This summary is machine-generated.

Preclinical models of joint inflammation, including K/BxN and collagen-induced arthritis, are crucial for evaluating autoimmune diseases. These models aid in testing immunotherapies and understanding genetic contributions to autoimmune conditions.

Keywords:
AutoantibodiesAutoimmunityImmune related adverse eventsMouse modelsRheumatoid arthritis

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Area of Science:

  • Immunology
  • Rheumatology
  • Preclinical Research

Background:

  • Autoimmune diseases are increasing, necessitating evaluation in preclinical models.
  • Immunotherapies may cause autoimmune side effects, requiring careful assessment.
  • Rheumatic diseases are common autoimmune conditions impacting joints.

Purpose of the Study:

  • To describe common murine models of joint inflammation for autoimmunity research.
  • To highlight the utility of K/BxN and collagen-induced arthritis models.
  • To provide tools for evaluating immunotherapies and genetic factors in autoimmune disease.

Main Methods:

  • Description of the K/BxN T cell transgenic model of autoimmune arthritis.
  • Explanation of arthritis induction methods in K/BxN models (spontaneous, serum transfer, adoptive transfer).
  • Overview of the collagen-induced arthritis model.

Main Results:

  • The K/BxN model offers rapid, synchronous, and highly penetrant arthritis development.
  • K/BxN arthritis can be induced via multiple methods.
  • Both K/BxN and collagen-induced arthritis models are suitable for therapy testing.

Conclusions:

  • The K/BxN model, with its C57BL/6 background, is advantageous for genetic studies.
  • These murine models are valuable for assessing autoimmune side effects of therapies like monoclonal antibodies and nanotherapies.
  • The described models can help elucidate genetic contributions to autoimmune diseases.