Concanavalin A Model
Concanavalin A Model - Related Videos
04:02
Ultrasound-Guided Concanavalin A Injection Into Inferior Lacrimal Gland: A Technique to Inoculate Inferior Lacrimal Gland With Concanavalin A to Induce Dry Eye Disease in Rabbit Model
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2025
In this video, we demonstrate the inoculation of Concanavalin A, a lymphocyte mitogen, into the inferior lacrimal gland of the eye of a rabbit to induce dry eye disease. Ultrasound or sonogram images are used to guide the precise location of the injection site and also to confirm the success of inoculation.
09:07
Concanavalin A-Based Sedimentation Assay to Measure Substrate Binding of Glucan Phosphatases
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2022
This method describes a lectin-based in vitro sedimentation assay to quantify the binding affinity of glucan phosphatase and amylopectin. This co-sedimentation assay is reliable for measuring glucan phosphatase substrate binding and can be applied to various solubilized glucan substrates.
08:04
A Rabbit Model of Aqueous-Deficient Dry Eye Disease Induced by Concanavalin A Injection into the Lacrimal Glands: Application to Drug Efficacy Studies
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Cited by 12 •
2020
This article describes the development of a method to induce acute or chronic dry eye disease in rabbits by injecting concanavalin A to all portions of the orbital lacrimal gland system. This method, superior to those already reported, generates a reproducible, stable model of dry eye suitable for the study of pharmacological agents.
02:54
Performing Injection into Palpebral Portion of the Superior Lacrimal Gland: A Technique for Inducing Dry Eye Disease in Rabbit Model
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2025
In this video, we show a procedure to induce aqueous-deficient dry eye disease in a rabbit model by injecting the palpebral portion of the superior lacrimal gland with Concanavalin A. This model is useful for pharmacokinetic and biodistribution assays of drugs for treating dry eye disease.
12:31
In Vivo Modeling of the Morbid Human Genome using Danio rerio
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Cited by 66 •
2013
Here, we present a systematic approach for developing physiologically relevant, sensitive and specific in vivo assays for interpreting variation in human pathology. Transient genetic manipulation via microinjection of WT and mutant human mRNA and morpholino (MO) antisense oligonucleotides harness the tractability of the developing zebrafish embryo to rapidly assay pathogenic mutations, especially, but not exclusively, in the context of human developmental disorders.
FAQs
The initiating event is lectin-mediated cross-linking of T-cell receptors. This activates lymphocytes, which then release cytokines that coordinate and amplify inflammation. The resulting signaling links a defined immune stimulus to downstream liver injury, allowing investigators to examine how T-cell activation can progress from receptor engagement to tissue damage.
Cytokines and infiltrating immune cells provide complementary mechanisms of injury. Cytokine release helps sustain inflammatory signaling, while recruited cells enter liver tissue and contribute to hepatocyte damage. Examining these events together helps distinguish an initial activation signal from later tissue-level consequences, an important distinction when evaluating immune-mediated liver inflammation.
The model connects adaptive immune activation with innate inflammatory responses in the liver. T-cell receptor engagement initiates lymphocyte activation, while the resulting inflammatory environment involves broader immune participation and tissue injury. This linkage helps medical researchers study how different arms of immunity cooperate during liver inflammation rather than examining either response in isolation.
Hepatocyte damage provides a tissue-level readout of the immune response rather than merely showing that lymphocytes became activated. Comparing immune signaling with the extent of cellular injury helps investigators relate mechanism to disease consequence. That relationship is useful for studying inflammatory injury and for assessing whether an intervention may limit liver damage.
The experimental sequence follows the consequences of administration from lymphocyte activation through cytokine release, immune-cell infiltration, and hepatocyte damage. This progression gives researchers a framework for connecting an initiating immune stimulus with measurable inflammatory injury. Focusing on the sequence also supports comparisons between immune activation, tissue damage, and subsequent repair-related questions.
Researchers can apply candidate immunomodulatory drugs within this experimentally induced inflammatory setting and compare how the immune response and liver injury change. The model therefore provides a platform for testing whether an intervention affects cytokine-driven inflammation, immune-cell involvement, or hepatocyte damage. These comparisons help prioritize treatments and clarify their potential mechanisms.
In medicine, the model helps investigate immune mechanisms relevant to autoimmune hepatitis while also supporting broader studies of inflammatory liver injury. Researchers can use it to identify therapeutic targets and compare mechanisms of tissue injury and repair. Its value lies in linking immune activity with liver outcomes that matter for disease treatment and recovery.