Collagen-induced Arthritis
Collagen-induced Arthritis - Related Videos
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.
09:31
Generation of Induced-pluripotent Stem Cells Using Fibroblast-like Synoviocytes Isolated from Joints of Rheumatoid Arthritis Patients
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Cited by 13 •
2016
Here we describe a protocol for generating human induced-pluripotent stem cells from patient-derived fibroblast-like synoviocytes, using a lentiviral system without feeder cells.
05:42
A Turbidimetric Analysis to Monitor Collagen-Induced Aggregation of Pretreated Human Platelets
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2025
This video demonstrates turbidimetric analysis to assess collagen-induced platelet aggregation in pre-treated, washed human platelets. Control wells show collagen-induced aggregation, whereas a high concentration of inhibitors blocks Pannexin-1 channels, thereby inhibiting collagen-induced platelet aggregation, evident from unchanged turbidity.
11:03
A Cryo-pulverization Protocol for Processing Mouse Paws to Evaluate Molecular Pathways of Tissue Inflammation in a Collagen Induced Arthritis Model
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2019
A cryogenic pulverization method to process murine paws using a liquid nitrogen freezer mill was developed to improve the yield and quality of RNA or protein extracted from the tissues and enable the analysis of molecular profiles associated with inflammatory responses.
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...
FAQs
Disease development depends partly on whether an animal is susceptible to the experimental autoimmune response. Type II collagen is commonly administered with an adjuvant, which helps initiate immune activation against the collagen-associated target. Comparing susceptible and less-susceptible animals allows investigators to examine how genetic background shapes antigen-specific immunity and the likelihood of inflammatory joint disease.
Type II collagen immunization activates collagen-specific T and B cells rather than producing only a nonspecific inflammatory reaction. B-cell responses generate autoantibodies, while T-cell activity contributes to antigen-specific immune coordination. Studying these linked responses helps researchers separate adaptive immune contributions and determine how recognition of collagen is associated with subsequent joint inflammation.
Cytokine networks help connect immune activation with the inflammatory processes occurring in the joints. Their study places antigen-specific T- and B-cell responses within a broader interaction between innate and adaptive immunity. This perspective is useful for identifying how coordinated immune signals may influence disease intensity, inflammatory damage, and the effects of candidate interventions.
Joint inflammation in this model is examined not only as an immune-cell response but also as tissue damage affecting cartilage and bone. Linking immune activity with these structural outcomes helps investigators evaluate whether a treatment merely reduces inflammation or also limits destructive disease consequences. This makes tissue injury an important outcome alongside immune and cytokine measurements.
The central procedure is immunization of susceptible animals with type II collagen, often delivered in an adjuvant. This exposure initiates the collagen-directed immune response that investigators then follow as joint inflammation and tissue damage develop. The overview supports this immunization framework, but it does not specify doses, administration routes, schedules, or particular methods for assessing disease.
Investigators can use the system to examine genetic susceptibility, antigen-specific immunity, cytokine networks, and the relationship between innate and adaptive immune responses. It also supports analysis of cartilage and bone destruction. Because these questions span immune mechanisms and tissue outcomes, the model provides a framework for connecting immunology with the pathology of inflammatory joint disease.
The model provides a preclinical setting for evaluating anti-inflammatory and disease-modifying therapies before clinical investigation. Researchers can examine whether candidate treatments alter immune-mediated joint inflammation and associated cartilage or bone damage. Its value lies in testing therapeutic effects within an experimental autoimmune response that includes antigen-specific immunity, autoantibodies, and coordinated innate and adaptive mechanisms.