Murine Arthritis Models
Murine Arthritis Models - Related Videos
03:52
A Cell-Based Therapy for Autoimmune Arthritis in a Murine Model
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2025
This video showcases a cell-based therapy for autoimmune arthritis in mice. iPSC-derived T regulatory cells expressing ovalbumin-specific receptors are injected with methylated bovine serum albumin (mBSA) emulsified in an adjuvant. Murine antigen-presenting cells (APCs) process and present the mBSA to T cells, prompting T cell activation and migration to the knee joint's synovial membrane. Subsequent injections involve mBSA alone in the left knee and a combination of mBSA and ovalbumin in the...
03:29
A Technique to Generate an Adjuvant-Induced Arthritis Mouse Model
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2025
This video demonstrates a method to generate adjuvant-induced arthritis in a murine model. Complete Freund's adjuvant (CFA) is injected in the mouse ankle joint and periarticular areas. CFA activates the immune system, leading to neutrophil infiltration and exaggerated inflammation.
04:35
Murine Ileal Resection Model: Studying Ileectomy-Induced Bile Metabolism in Murine Model
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2023
This video describes the detailed protocol for intestinal resection in a murine model. This technique provides insights into ileectomy-induced bile malabsorption, overaccumulation, and toxicity in the mouse intestine.
09:04
In Vivo Optical Imaging of Brain Tumors and Arthritis Using Fluorescent SapC-DOPS Nanovesicles
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Cited by 13 •
2014
We describe a multi-angle rotational optical imaging (MAROI) system for in vivo quantitation of a fluorescent marker delivered by saposin C (SapC)-dioleoylphosphatidylserine (DOPS) nanovesicles. Employing mouse models of cancer and arthritis, we demonstrate how the MAROI signal curve analysis can be used for the precise mapping and biological characterization of disease processes.
07:15
In vivo Macrophage Imaging Using MR Targeted Contrast Agent for Longitudinal Evaluation of Septic Arthritis
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Cited by 2 •
2013
We demonstrate how to perform macrophage MR imaging using ultrasmall superparamagnetic contrast agent (USPIO) in septic arthritis, allowing an initial and longitudinal in vivo non-invasive evaluation of macrophages infiltration and an assessment of therapy efficacy.
FAQs
The induction route determines which immune event initiates joint pathology. Immunization with joint-associated antigens models antigen-driven activation, arthritogenic antibodies emphasize antibody-mediated disease, and transfer of activated immune cells tests the effects of pathogenic cellular immunity. Comparing these routes helps investigators connect the initiating mechanism with downstream synovial inflammation, cartilage degradation, and bone erosion.
These components provide connected levels for analyzing disease progression. Immune cells and cytokines contribute to inflammatory signaling, synovial tissue reflects local joint inflammation, and cartilage and bone reveal structural damage. Studying them together helps researchers determine how immune activity becomes tissue injury rather than evaluating inflammation or skeletal damage as isolated outcomes.
Genetic flexibility allows investigators to examine how inherited biological differences affect inflammatory and autoimmune joint disease. It also supports controlled comparisons among experimental systems while keeping the disease stimulus and measurable outcomes defined. This feature is especially valuable when researchers want to investigate mechanisms, biomarkers, or treatment responses in a reproducible laboratory setting.
No single mouse system reproduces every feature of human arthritis. Each model captures selected aspects of pathogenesis, inflammation, tissue damage, or immune activity under controlled conditions, so results require careful interpretation. Their main value is translational: they clarify mechanisms and identify promising biomarkers or therapies that can then be evaluated for relevance to human disease.
Researchers first select an induction approach that matches the immune mechanism under investigation, using joint-associated antigens, arthritogenic antibodies, or activated immune cells. They then follow disease development through clinical and tissue-related outcomes, examine biomarkers, and assess a therapeutic candidate or biological mechanism. This sequence connects experimental cause with inflammation, structural damage, and treatment response.
Useful outcomes include synovial inflammation, cartilage degradation, and bone erosion, together with disease biomarkers and observable clinical changes. Examining these endpoints in combination reveals both inflammatory activity and structural consequences in the joint. The resulting profile can help investigators compare disease mechanisms, evaluate tissue damage, and determine whether a therapeutic candidate changes the experimental disease course.
They are particularly useful when researchers need a controlled system for studying autoimmune or inflammatory joint-disease mechanisms, testing therapeutic candidates, or examining links among immune responses, cytokines, synovium, cartilage, and bone. Their measurable outcomes and genetic flexibility support translational research in rheumatology, while their limitations require findings to be interpreted alongside the complexity of human arthritis.