Genetically Driven Autoimmunity
Genetically Driven Autoimmunity - Related Videos
09:23
Parasite Induced Genetically Driven Autoimmune Chagas Heart Disease in the Chicken Model
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Cited by 12 •
2012
The inoculation of Trypanosoma cruzi in fertile eggs prior to incubation renders the parasite kDNA minicircle integration in embryo cells genome. Crossbreeding reveals the vertical transfer of the mutations to progeny. The kDNA integrates into coding regions at several chromosomes and the chickens die with an inflammatory autoimmune heart disease.
09:03
The CYP2D6 Animal Model: How to Induce Autoimmune Hepatitis in Mice
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Cited by 31 •
2012
Infection of mice with an Adenovirus expressing the major human autoantigen cytochrome P450 2D6 (hCYP2D6) recognized by sera of patients suffering from type 2 autoimmune hepatitis results in a persistent form of autoimmune-mediated liver disease characterized by extensive hepatitis, fibrosis and generation of a CYP2D6-specific immune response.
10:38
Induction of Experimental Autoimmune Hypophysitis in SJL Mice
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Cited by 4 •
2010
This video shows how to induce autoimmune hypophysitis in SJL mice and how to assess its severity by histopathology.
09:58
Light-driven Enzymatic Decarboxylation
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Cited by 6 •
2016
We describe a protocol for the light-catalyzed generation of hydrogen peroxide — a cofactor for oxidative transformations.
02:27
Induction of Experimental Autoimmune Encephalomyelitis in a Mouse Model
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2025
In this video, a mouse model of multiple sclerosis is established using experimental autoimmune encephalomyelitis (EAE). The mouse is injected with an emulsion containing a neuronal peptide and an adjuvant, triggering an immune response that activates autoreactive T cells. This is followed by an injection of pertussis toxin (PTX) to increase blood-brain barrier permeability, allowing the autoreactive T-cells to infiltrate the brain. This infiltration initiates a signaling cascade that...
FAQs
Variants that affect lymphocyte selection can allow self-reactive immune cells to escape the processes that normally remove or control them. These cells may then persist in the immune system and contribute to tissue damage when activated. Examining this checkpoint helps explain how genetic differences alter self-tolerance and why autoimmune susceptibility can cluster within families.
Regulatory T cells help maintain immune restraint, while cytokine pathways coordinate inflammatory signaling. Inherited changes affecting either system can weaken suppression or intensify inflammatory responses, making harmful immune activity more likely to persist. Studying both components helps distinguish whether a condition primarily reflects failed regulation, excessive signaling, or interaction between these mechanisms.
An infection may act as an environmental trigger, but inherited immune-regulatory variants influence how an individual responds to that challenge. Differences in antigen recognition, inflammatory signaling, or clearance of cellular debris can therefore lead to different outcomes among people exposed to similar infections. This interaction is central to studying autoimmunity within immunology and infection research.
Genetic insights can identify inherited differences associated with altered immune regulation, antigen recognition, or inflammatory signaling. This information supports risk assessment by helping investigators and clinicians interpret why autoimmune conditions may cluster in families. Genetic findings do not replace immune or clinical evaluation, but they can provide context for understanding susceptibility and variation in disease development.
Disease classification can incorporate the biological pathway affected by inherited variation, such as lymphocyte selection, regulatory T-cell activity, cytokine signaling, or cellular-debris clearance. Organizing conditions by these mechanisms may clarify why apparently similar autoimmune diseases differ in immune behavior. It also creates a framework for connecting genetic findings with disease patterns and potential treatment strategies.
Identifying the disrupted immune pathway can indicate whether treatment should focus on restoring immune regulation or limiting harmful inflammation. For example, findings involving regulatory control, cytokine signaling, or debris clearance can help frame pathway-specific therapeutic goals. In this context, genetic analysis supports targeted therapy development rather than relying only on broad suppression of immune activity.