Autoimmune Destruction
Autoimmune Destruction - Related Videos
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.
09:03
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.
08:24
Introduction to the Ultrasound Targeted Microbubble Destruction Technique
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Cited by 19 •
2011
Ultrasound Targeted Microbubble Destruction (UTMD) can be used to direct site-specific delivery of bioactive molecules, including therapeutic genes, to target organs accessible to ultrasound, such as the heart and liver1-6.
04:08
Preparing an Antigen-Adjuvant Emulsion to Induce Autoimmune Encephalomyelitis
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2025
This video demonstrates an efficient homogenization technique to generate an antigen-adjuvant emulsion to induce experimental autoimmune encephalomyelitis (EAE) in a murine model. The emulsion contains an autoantigen — myelin oligodendrocyte glycoprotein (MOG) — in the water phase, surrounded by a continuous oil phase comprising an inactivated pathogenic bacteria. The emulsion ensures a sustained release of antigens for a prolonged immune response.
01:12
Non-destructive Tests for Concrete Strength
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2024
The rebound hammer test, also known as the Schmidt hammer test, is a non-destructive technique for evaluating the hardness of concrete and, indirectly, the strength of concrete. It operates on the principle that the rebound of a spring-driven mass from a concrete surface correlates to the surface's hardness. The device comprises a mass within a tubular housing, a spring mechanism, and a plunger that strikes the concrete. Upon release, the energy imparted to the mass by the spring causes it to...
FAQs
When self-tolerance fails, autoreactive T cells and autoantibodies can identify normal self-antigens as targets. This recognition starts immune activity against the body’s own cells, tissues, or organs rather than against an external threat. The resulting response provides the mechanistic basis for studying which immune signals and target structures might be interrupted pharmacologically.
Autoreactive T cells and autoantibodies contribute through different immune routes. T cells can promote inflammation or directly kill target cells through cytotoxic pathways, while autoantibodies can recognize self-antigens and help activate complement. Distinguishing these contributors matters because drug development can focus on reducing immune activation, inflammatory signaling, or the damaging pathway most relevant to the disease.
These processes represent separate mechanisms through which immune recognition becomes tissue injury. Inflammation amplifies local immune activity, complement activation adds another route of damage, and cytotoxic pathways can directly eliminate target cells. Identifying the dominant mechanism helps pharmacologists connect the biology of autoimmune destruction with treatments intended to suppress immune activity or block specific inflammatory signals.
The disease mechanism involves harmful immune activity directed toward self, whereas treatment must reduce that activity without unnecessarily disabling protective immune functions. Broad immune suppression may control autoimmune injury but can also produce infections, toxicity, and other unwanted effects. This contrast explains the pharmacological emphasis on more selective interventions that act on relevant immune or inflammatory pathways.
Corticosteroids, immunosuppressants, and targeted biologic therapies are the principal treatment approaches identified for this context. Corticosteroids and immunosuppressants reduce immune activity broadly, while targeted biologics are used to block inflammatory signaling more selectively. Their shared purpose is to limit immune-mediated injury, but their differing degrees of selectivity shape therapeutic development and safety considerations.
Targeted biologic therapies address autoimmune injury by blocking inflammatory signaling rather than relying only on broad reduction of immune activity. This approach reflects an effort to intervene at a more specific point in the disease mechanism. In pharmacology, such selectivity is important because it may help control disease while reducing infections, toxicity, and other effects associated with wider immune suppression.
Selective drug development seeks to separate disease control from unnecessary disruption of immune function. Researchers use knowledge of autoreactive T cells, autoantibodies, complement, cytotoxic pathways, and inflammatory signaling to identify more focused intervention points. The desired outcome is effective suppression of autoimmune injury with fewer infections, toxicities, and other consequences than may accompany broad immune suppression.