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Autoimmune diseases are a group of disorders in which the body's immune system mistakenly attacks its own cells, tissues, and organs. This results from an overactive immune response against substances and tissues normally present in the body. Let's delve into the concept and mechanism of autoimmune diseases from an immune system point of view, explore different causes and examples of such diseases, and discuss potential solutions.
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Adrenergic Receptors: ɑ Subtype01:31

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Adrenoceptors are classified into α and ꞵ classes based on their potencies to catecholamine agonists. α-adrenoceptors show the following order of catecholamine potency:
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An aortic aneurysm is a localized outpouching or dilation at a weak point in the artery wall. It may involve different parts of the aorta, such as the abdominal aorta, aortic arch, or thoracic aorta.Etiological factorsSeveral disorders are associated with aortic aneurysms.Congenital causes, such as primary connective tissue disorders like Marfan syndrome, impact the integrity and strength of connective tissues, notably affecting the aorta. Marfan syndrome is a genetic disorder that specifically...
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Asthma is a chronic pulmonary condition involving inflammation of the airways, hyper-reactivity, and reversible obstruction of the airways. This condition can significantly impact a person's quality of life, making breathing difficult and leading to distressing symptoms.
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Related Experiment Video

Updated: Jan 4, 2026

Isolation of Human Lymphatic Endothelial Cells by Multi-parameter Fluorescence-activated Cell Sorting
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Hereditary and acquired angioedema.

Gayatri Patel, Jacqueline A Pongracic

    Allergy and Asthma Proceedings
    |November 7, 2019
    PubMed
    Summary

    Hereditary angioedema (HAE) is a genetic disorder caused by C1 esterase inhibitor (C1-INH) deficiency. New therapies offer effective on-demand and prophylactic treatments for HAE management.

    Area of Science:

    • Immunology
    • Genetics
    • Pharmacology

    Background:

    • Hereditary angioedema (HAE) is an autosomal dominant disorder resulting from C1 esterase inhibitor (C1-INH) deficiency.
    • Acquired angioedema involves C1-INH consumption (Type 1) or inactivation (Type 2), both potentially life-threatening.
    • HAE types include Type 1 (85%, low C1-INH production), Type 2 (15%, dysfunctional C1-INH), and rare HAE with normal C1-INH.

    Purpose of the Study:

    • To review the classification, diagnosis, and evolving therapeutic landscape of Hereditary Angioedema (HAE).
    • To highlight the diagnostic utility of complement components C4 and C1q in differentiating HAE subtypes and acquired angioedema.
    • To discuss the impact of novel, disease-specific therapies on HAE management.

    Main Methods:

    • Review of literature on HAE classification, pathophysiology, and diagnostic markers.

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  • Analysis of current on-demand and long-term prophylactic treatment options for HAE.
  • Discussion of genetic mutations associated with HAE, including Factor XII, angiopoietin-1, and plasminogen.

    • Main Results:

    • Complement component C4 is typically low in HAE types 1 and 2, aiding diagnosis.
    • C1q protein levels help differentiate HAE (normal) from acquired angioedema (low).
    • Disease-specific therapies, including plasma/recombinant C1-INH, kallikrein inhibitors, and bradykinin antagonists, have transformed HAE management.

    Conclusions:

    • HAE management has been significantly improved by targeted therapies for both acute attacks and prophylaxis.
    • Accurate diagnosis, supported by C4 and C1q levels, is crucial for appropriate HAE treatment.
    • Advances in understanding HAE genetics and pathophysiology continue to drive therapeutic innovation.