• Save
Hypersensitivity and autoimmune diseases
Upcoming SlideShare
Loading in...5

Hypersensitivity and autoimmune diseases



for Gen Path Lecture (prefinal)

for Gen Path Lecture (prefinal)



Total Views
Slideshare-icon Views on SlideShare
Embed Views



0 Embeds 0

No embeds


Upload Details

Uploaded via as Microsoft PowerPoint

Usage Rights

© All Rights Reserved

Report content

Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.


11 of 1

  • Full Name Full Name Comment goes here.
    Are you sure you want to
    Your message goes here
Post Comment
Edit your comment

    Hypersensitivity and autoimmune diseases Hypersensitivity and autoimmune diseases Presentation Transcript

    • Hypersensitivity and autoimmune diseases
    • • Medical news reports a rise of hypersensitivity reactions to various foodstuffs, particles and even personal stuff. In what 3 ways do you think would help you as well as the patient in preventing catastrophic events arising from hypersensitivity reactions in the dental clinic?
    • Hypersensitivity • The phenomenon of damage caused by the immune system while trying to combat an insult. • Precipitating factor (external), instead of the immune system coping and restoring the body’s homeostasis, the immune response is altered and becomes the “internal” cause of disease.
    • Type I hypersensitivity • Anaphylactic • Release of allergic mediators • Asthma, eczema, hay fever and reactions to certain food • Grass pollen, house dust mite feces or seafoods
    • • Immediate injections of epinephrine • Antihistamine or steroids as back up medications • Avoidance of allergens
    • Type II hypersensitivity • Antibody dependent cytotoxic hypersensitivity • Antibodies react with antigens fixed to the surface of various types of cells and cause damage • Complement fixing (the antibodies cause the destruction of the target cell or damage the surrounding cells)
    • • Functional fixing (antibodies interfere with cell function) • Drug reactions where a binding of a drug may alter a normal self antigen and thus produce something that can no longer be tolerated
    • Type II hypersensitivity - Rhesus incompatibility
    • Type III hypersensitivity • Immune complex mediated hypersensitivity • Antibody driven process • The antibodies react with free antigen and under the right circumstances they form soluble immune complexes that circulate in the blood giving rise to “serum sickness”
    • Type III hypersensitivity – Farmer’s Lung Alveolitis
    • Type IV hypersensitivity • Cell mediated (delayed type) hypersensitivity • T lymphocytes which over several hours and days recruit and activate other T cells and macrophages and produce local tissue damage and granuloma formation
    • Type IV hypersensitivity – Mantoux Test
    • Autoimmune Diseases General Principles • Autoimmunity arises through some combination of susceptibility genes (causing loss of self tolerance) and environmental triggers (specially infection)
    • • Self antigens or abnormal immune cells develop that incite the immune response into abnormal or excessive activity of T or B lymphocytes • Once induced tend to be progressive, albeit with occasional relapses and remissions
    • • Most autoimmune disorders are complex multigenic disorders - associated with specific histocompatibility molecule HLA alleles - defects in pathways that normally regulate either peripheral or central tolerance - polymorphisms in other genes (PTPN- 22, NOD-2, IL-2 and IL-7) • Role of infection
    • • GI: primary biliary cirrhosis, ulcerative colitis and atrophic gastritis • Cardiovascular: pernicious anemia, hemolytic anemia, idiopathic thrombocytopenia and leukopenia • Endocrine: insulin dependent diabetes, thyrotoxicosis and Hashimoto’s thyroiditis • Musculoskeletal: mixed connective tissue diseases, rheumatoid arthritis, systemic lupus erythematosus, myasthenia gravis • Dermatology: dermatomyositis and scleroderma
    • Rejection of Tissue Transplants • Mechanisms of recognition: - Class I molecules are expressed on all nucleated cells. Class I molecules bind peptide fragments derived from endogenous proteins - Class II molecules are confined to APC including dendritic cells, macrophages, B cells and activated T cells
    • - Class II molecules bind peptide fragments derived from exogenous proteins and presents these processed antigens to CD4+ T lymphocytes • Host T cells recognize either by direct or indirect pathways
    • Rejection of solid organs: • Following lymphocyte activation, rejection is mediated by the following: - direct CTL-mediated parenchymal and endothelial cytolysis - macrophage mediated damage - cytokine mediated vascular and parenchymal dysfunction - microvasccular injury - antibody mediated responses
    • • Rejection: - hyperacute - acute - chronic
    • Immunodeficiency Syndrome • Primary immunodeficiencies - are usually hereditary and manifest between 6 months and 2 years of life as maternal protection is lost • Secondary immunodeficiencies - result from altered immune function due to infections, malnutrition, aging, immunosuppression, irradiation, chemotherapy and autoimmunity
    • • Acquired immunodeficiency syndrome - retrovirus human immunodeficiency virus (HIV) characterized by profound suppression of T cell mediated immunity leading to opportunistic infections, secondary neoplasms and neurologic disorders
    • Amyloidosis • Amyloid is a heterogenous group of fibrillar proteins that share the ability to aggregate into an insoluble, cross-beta pleated sheet tertiary conformation • Amyloid fibrils accumulate extracellularly in tissues due either to excess synthesis or resistance to catabolism
    • • As amyloid accumulates, it produces pressure atrophy of adjacent parenchyma • Depending on tissue distribution and degree of involvement, the clinical effects of amyloid can range from life threatening to an asymptomatic incidental finding at autopsy
    • Do you have any questions?