Collagen-induced arthritis: Difference between revisions
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{{Infobox medical condition | |||
| name = Collagen-induced arthritis | |||
| synonyms = CIA | |||
| field = [[Rheumatology]] | |||
| symptoms = [[Joint pain]], [[swelling]], [[stiffness]] | |||
| complications = [[Chronic pain]], [[joint damage]] | |||
| onset = Typically induced in laboratory settings | |||
| duration = Variable, depending on experimental conditions | |||
| causes = [[Autoimmune response]] to type II [[collagen]] | |||
| risks = Used primarily in [[animal models]] | |||
| diagnosis = Based on [[clinical signs]] and [[histopathology]] | |||
| differential = [[Rheumatoid arthritis]], [[osteoarthritis]] | |||
| treatment = Experimental treatments, [[immunosuppressive therapy]] | |||
| prognosis = Depends on experimental intervention | |||
| frequency = Commonly used in [[research]] settings | |||
}} | |||
{{Short description|An animal model of rheumatoid arthritis}} | {{Short description|An animal model of rheumatoid arthritis}} | ||
'''Collagen-induced arthritis''' (CIA) is an experimental model of [[rheumatoid arthritis]] (RA) that is commonly used in [[immunology]] and [[rheumatology]] research. This model is primarily used to study the pathogenesis of RA and to evaluate potential therapeutic interventions. | '''Collagen-induced arthritis''' (CIA) is an experimental model of [[rheumatoid arthritis]] (RA) that is commonly used in [[immunology]] and [[rheumatology]] research. This model is primarily used to study the pathogenesis of RA and to evaluate potential therapeutic interventions. | ||
==Overview== | ==Overview== | ||
Collagen-induced arthritis is induced in susceptible strains of [[laboratory animals]], such as [[mice]] and [[rats]], by immunization with [[type II collagen]], which is a major component of [[articular cartilage]]. The model is characterized by the development of an [[autoimmune]] response against type II collagen, leading to [[inflammation]] and [[joint destruction]] similar to that seen in human rheumatoid arthritis. | Collagen-induced arthritis is induced in susceptible strains of [[laboratory animals]], such as [[mice]] and [[rats]], by immunization with [[type II collagen]], which is a major component of [[articular cartilage]]. The model is characterized by the development of an [[autoimmune]] response against type II collagen, leading to [[inflammation]] and [[joint destruction]] similar to that seen in human rheumatoid arthritis. | ||
==Pathogenesis== | ==Pathogenesis== | ||
The pathogenesis of collagen-induced arthritis involves both [[innate immunity|innate]] and [[adaptive immunity|adaptive]] immune responses. The initial immunization with type II collagen, often emulsified in [[Freund's adjuvant]], leads to the activation of [[T cells]] and [[B cells]]. These immune cells produce [[cytokines]] and [[autoantibodies]] that contribute to the inflammatory process and joint damage. | The pathogenesis of collagen-induced arthritis involves both [[innate immunity|innate]] and [[adaptive immunity|adaptive]] immune responses. The initial immunization with type II collagen, often emulsified in [[Freund's adjuvant]], leads to the activation of [[T cells]] and [[B cells]]. These immune cells produce [[cytokines]] and [[autoantibodies]] that contribute to the inflammatory process and joint damage. | ||
===Role of T Cells=== | ===Role of T Cells=== | ||
[[CD4+ T cells]], particularly the [[Th1]] and [[Th17]] subsets, play a crucial role in the development of CIA. These cells produce pro-inflammatory cytokines such as [[interferon-gamma]] (IFN- | [[CD4+ T cells]], particularly the [[Th1]] and [[Th17]] subsets, play a crucial role in the development of CIA. These cells produce pro-inflammatory cytokines such as [[interferon-gamma]] (IFN-γ) and [[interleukin-17]] (IL-17), which promote the recruitment and activation of other immune cells in the joints. | ||
===Role of B Cells=== | ===Role of B Cells=== | ||
B cells contribute to the pathogenesis of CIA by producing [[autoantibodies]] against type II collagen. These autoantibodies form immune complexes that deposit in the joints, leading to [[complement system|complement activation]] and further inflammation. | B cells contribute to the pathogenesis of CIA by producing [[autoantibodies]] against type II collagen. These autoantibodies form immune complexes that deposit in the joints, leading to [[complement system|complement activation]] and further inflammation. | ||
==Clinical Features== | ==Clinical Features== | ||
The clinical features of collagen-induced arthritis in animal models include [[joint swelling]], [[erythema]], and [[reduced mobility]]. Histologically, affected joints show [[synovitis]], [[pannus formation]], and [[cartilage]] and [[bone erosion]]. These features closely mimic those observed in human rheumatoid arthritis. | The clinical features of collagen-induced arthritis in animal models include [[joint swelling]], [[erythema]], and [[reduced mobility]]. Histologically, affected joints show [[synovitis]], [[pannus formation]], and [[cartilage]] and [[bone erosion]]. These features closely mimic those observed in human rheumatoid arthritis. | ||
==Research Applications== | ==Research Applications== | ||
Collagen-induced arthritis is widely used in preclinical studies to evaluate the efficacy of new [[anti-inflammatory]] and [[immunosuppressive]] drugs. It is also used to study the mechanisms of [[autoimmunity]] and the role of specific immune cells and cytokines in the pathogenesis of arthritis. | Collagen-induced arthritis is widely used in preclinical studies to evaluate the efficacy of new [[anti-inflammatory]] and [[immunosuppressive]] drugs. It is also used to study the mechanisms of [[autoimmunity]] and the role of specific immune cells and cytokines in the pathogenesis of arthritis. | ||
==Limitations== | ==Limitations== | ||
While CIA is a valuable model for studying rheumatoid arthritis, it has limitations. The model does not fully replicate the complexity of human RA, and the genetic and environmental factors that contribute to RA in humans are not fully represented in the animal model. | While CIA is a valuable model for studying rheumatoid arthritis, it has limitations. The model does not fully replicate the complexity of human RA, and the genetic and environmental factors that contribute to RA in humans are not fully represented in the animal model. | ||
==Related pages== | ==Related pages== | ||
* [[Rheumatoid arthritis]] | * [[Rheumatoid arthritis]] | ||
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* [[Immunology]] | * [[Immunology]] | ||
* [[Animal model]] | * [[Animal model]] | ||
[[Category:Autoimmune diseases]] | [[Category:Autoimmune diseases]] | ||
[[Category:Animal testing]] | [[Category:Animal testing]] | ||
[[Category:Immunology]] | [[Category:Immunology]] | ||
Latest revision as of 06:10, 4 April 2025
| Collagen-induced arthritis | |
|---|---|
| Synonyms | CIA |
| Pronounce | N/A |
| Specialty | N/A |
| Symptoms | Joint pain, swelling, stiffness |
| Complications | Chronic pain, joint damage |
| Onset | Typically induced in laboratory settings |
| Duration | Variable, depending on experimental conditions |
| Types | N/A |
| Causes | Autoimmune response to type II collagen |
| Risks | Used primarily in animal models |
| Diagnosis | Based on clinical signs and histopathology |
| Differential diagnosis | Rheumatoid arthritis, osteoarthritis |
| Prevention | N/A |
| Treatment | Experimental treatments, immunosuppressive therapy |
| Medication | N/A |
| Prognosis | Depends on experimental intervention |
| Frequency | Commonly used in research settings |
| Deaths | N/A |
An animal model of rheumatoid arthritis
Collagen-induced arthritis (CIA) is an experimental model of rheumatoid arthritis (RA) that is commonly used in immunology and rheumatology research. This model is primarily used to study the pathogenesis of RA and to evaluate potential therapeutic interventions.
Overview[edit]
Collagen-induced arthritis is induced in susceptible strains of laboratory animals, such as mice and rats, by immunization with type II collagen, which is a major component of articular cartilage. The model is characterized by the development of an autoimmune response against type II collagen, leading to inflammation and joint destruction similar to that seen in human rheumatoid arthritis.
Pathogenesis[edit]
The pathogenesis of collagen-induced arthritis involves both innate and adaptive immune responses. The initial immunization with type II collagen, often emulsified in Freund's adjuvant, leads to the activation of T cells and B cells. These immune cells produce cytokines and autoantibodies that contribute to the inflammatory process and joint damage.
Role of T Cells[edit]
CD4+ T cells, particularly the Th1 and Th17 subsets, play a crucial role in the development of CIA. These cells produce pro-inflammatory cytokines such as interferon-gamma (IFN-γ) and interleukin-17 (IL-17), which promote the recruitment and activation of other immune cells in the joints.
Role of B Cells[edit]
B cells contribute to the pathogenesis of CIA by producing autoantibodies against type II collagen. These autoantibodies form immune complexes that deposit in the joints, leading to complement activation and further inflammation.
Clinical Features[edit]
The clinical features of collagen-induced arthritis in animal models include joint swelling, erythema, and reduced mobility. Histologically, affected joints show synovitis, pannus formation, and cartilage and bone erosion. These features closely mimic those observed in human rheumatoid arthritis.
Research Applications[edit]
Collagen-induced arthritis is widely used in preclinical studies to evaluate the efficacy of new anti-inflammatory and immunosuppressive drugs. It is also used to study the mechanisms of autoimmunity and the role of specific immune cells and cytokines in the pathogenesis of arthritis.
Limitations[edit]
While CIA is a valuable model for studying rheumatoid arthritis, it has limitations. The model does not fully replicate the complexity of human RA, and the genetic and environmental factors that contribute to RA in humans are not fully represented in the animal model.
