115.7 Hypersensitivity and Autoimmune Diseases

Terms

Hypersensitivity: exaggerated immune response occurring on

subsequent contact with the same antigen causing inflammation

and tissue damage

Atopic antigens: Antigens that trigger the formation of IgE

Allergens: proteins that induce the release of large amounts of IgE

in response to a small concentration of the antigen (i.e., pollen,

dust mites)

Anaphylaxis: A life-threatening immune reaction resulting from the

release of large amounts of chemical mediators initially from

activated basophils and mast cells

Classes type

  • Type I = Anaphylaxis : immediate, humoral mediated

  • Type II = Cytotoxic : immediate, humoral mediated

  • Type III = Immune Complex : immediate, humoral mediated

  • Type IV = Cell mediated : delayed, cell mediated

Type 1 = Anaphylaxis

Mediator/Key reactant IgE

Mechanism = Individual becomes sensitized to the offending antigen

and produces IgE that attaches to the Fc receptor of mast

cells/basophils

Upon subsequent exposure to the same antigen, and

further mediated by complement (C3a, C5) the cells lyse

and their granules release pre-formed chemical

mediators—histamine, heparin, leukotrienes, etc

Examples of type 1

  • Hay fever

  • Asthma

  • Food allergies (peanuts, milk, shellfish)—most common

  • Bee stings: wasps, hornets-most common

  • Latex sensitivites

  • Drug sensitivities

  • Anaphylaxis

Type 1 (Systemic Anaphylaxis)

  • Increase blood vessel permeability

  • Smooth muscle contraction cause respiratory difficulties

  • Ex- Venom from bees and Wasps, Peanuts or peanut- derived components, shell fish, Antibiotics such as penicllin

Testing for type 1

  • Prick test

  • Intradermal test

  • Measurement if IgE levels

  • Total IgE (RIST)

  • allergen specific IgE(RAST)


Type 2 = Cytotoxic

Mediators/Key Reactants = IgG or IgM antibodies attach to cell-bound antigen/ Complement activated

Mechanism = IgG or IgM are produced in response to antigen on cell surfaces

Ex - transfusion, Hemolytic disease, Autoimmune hemolytic anemia, mmune Thrombocytopenic Purpura

Type 3 = Immune Complex : immediate, humoral mediated

Mediators/Key Reactants = Soluble IgG or IgM (not cell bound) / Complement activation

Mechanism = Immune complexes (antibody-antigen) are not effectively

removed by phagocytosis. They deposit in various tissues (heart/kidney), where they

activate complement. Anaphylatoxins (i.e., C3a) activate mast cells/basos that initiate

an inflammatory response causing tissue damage

EX - Serum sickness, Lung necrosis from a fungus, Aspergillus fumigatus, Systemic Lupus Erythematosus (SLE) Rheumatoid arthritis (RA)

Type 4 = Cell mediated : delayed, cell mediated

Mediator/Key Reactants = T-lymphocytes that activate macrophages/monocytes

Mechanism= T lymphs that were previously exposed to specific antigen release

cytokines. Cytokines attract macrophages/monocytes and induce an

inflammatory response with resulting tissue damage. Action is delayed (i.e., occurs 48-72 hours later)

Ex- contact dermatitis,

Tool= Mantoux test


Autoimmune diseases

  • Occurs when the immune army turns against itself instead of recognizing itself from nonself

  • Dysfunction of the immune system

  • Causes of autoimmunity not fully understood

  • affects 5–7% of the population

  • Two major groups = Organ specific - antigen restricted to one organ / Systemic - immune complexes

  • Organ Specific = Type I Diabetes Mellitus, Myasthenia Gravis, Grave’s Disease, Hashimoto’s Thyroiditis, Multiple Sclerosis

  • Systemic = Systemic Lupus Erythematosus, Rheumatoid Arthritis