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An introduction to IgE Antibody: Key Player in Autoimmune Diseases

Author: Candy Swift
by Candy Swift
Posted: Aug 09, 2022

The prevalence of autoimmune diseases is about 7-9% and can be divided into organ-specific diseases, such as type I diabetes, multiple sclerosis, inflammatory bowel disease, myasthenia gravis, Hashimoto's disease, and autoimmune uveitis, and systemic diseases, including systemic lupus erythematosus, rheumatoid arthritis, mixed connective tissue disease, systemic sclerosis, and Sjogren's syndrome.

The core of autoimmune diseases is impaired self-tolerance of the immune system. The immune tolerance acts differently in different diseases, for example, in malignant tumors and microbial infections, the weaker the tolerance and the stronger the immune attack, the better for patients, while in allergic diseases, autoimmune diseases, organ transplants, etc., the stronger the tolerance, the better for human bodies.

Regulatory T cells (Tregs) play a central role in the prevention of autoimmune diseases by maintaining immune homeostasis and developing tolerance to autoantigens, and Tregs deficiency leads to elevated immunoglobulins, including autoimmune antibodies and IgE antibodies.

Immunoglobulin E (IgE), named in 1968, was the last of the five classes of human antibodies to be discovered, and today is commonly associated with the various manifestations of allergic disease. However, its role in mammalian evolution appears to be the provision of a mechanism for defense against parasites and animal venoms, and in this regard, it required the acquisition of a powerful effector function.

The mechanism of IgE antibodies in allergic diseases is well studied, simply put, dendritic cells present allergens to innate T cells (naive T cells), which causes differentiation of innate T cells into Th2 cells, activating B cells to produce allergen-specific IgE antibodies. These IgE antibodies bind to IgE high-affinity receptors on mast cells or basophils, causing cross-linking of IgE receptors and release of inflammatory factors, leading to the development of allergy.

In addition to allergic diseases, IgE antibodies may also be involved in the development of other diseases, including autoimmune diseases.

Some self-proteins in the body may be structurally similar to foreign proteins, and these self-proteins may then bind to specific antibodies to foreign allergens, leading to the development of disease. Other autoantigens that are not structurally similar to foreign allergens can lead to specific IgE antibodies, called autoreactive IgE, which can also lead to autoimmune disease.

Autoreactive IgE plays an important role in numerous autoimmune diseases, including lupus erythematosus, herpetiform aspergillosis, mixed connective tissue disease, Hashimoto's disease, and systemic sclerosis.

Anti-IgE therapy removes IgE from plasmacytoid dendritic cells (pDCs), reduces IgE-mediated cross-linking of IgE high-affinity receptors on pDCs, and restores Tregs homeostasis. Tregs ensure the body's immune homeostasis against foreign or autoantigens, and Tregs dysfunction leads to IgE autoantibodies. IgE autoantibodies cause autoimmune diseases by activating mast cells and basophils, so anti-IgE therapy may be able to treat such diseases by restoring the homeostasis of Tregs.

IgE differs from the various sub-classes of IgG that have hitherto been the common format for therapeutic antibodies in a number of key aspects, including its domain architecture, glycosylation, conformational dynamics, and, as only recently appreciated, allosteric properties. The function of IgE, as well as the possibility of understanding and harnessing it, makes it an attractive candidate for monoclonal antibody immunotherapy against clinically important targets.

About the Author

Candy Swift: Focus on the cutting edge biological information around the world.

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Author: Candy Swift
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Candy Swift

Member since: Nov 06, 2019
Published articles: 187

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