Hypersensitivity Reactions Flashcards
Which of the hypersensitivity reactions is Antibody Independent?
Type 4 Reaction
What is the 1st exposure/priming of a Type 1 hypersensitivity reaction?
This is when a Dendritic Cell presents an allergen to a Th0 Cell–> Th2 CELL–> Activates B Cells–> Secrete Ig E
IgE will bind to the Mast cells through ERIIA receptors to release histamines during second response
**There are no free immune complexes present; IgE will be bound to the mast cell (mast cells are found in perivascular connective tissue)
What is the 2nd exposure of a Type 2 hypersensitivity reaction like?
Allergen binds mast cells by IgE antibody for the second time. This results in a cascade of events which causes the release of:
- Neutrophil Chemotactic Factors
- Eosinophil Chemotactic Factors
- Proteases (to start complement cascade and results in tissue damage)
- Histamines: Vasodilation, increased permeability, glandular secretions
How does asthma occur?
Type I hypersensitivity reaction that occurs from the activation of mast cells within the bronchioles
Results in:
- ) Increased glandular secretion–> increased luminal obstruction via mucus
- ) mucosal and submucosal swelling
- ) Bronchioconstriction
What are the strongest vasodilating signals in the Type I hypersensitivity reaction?
Leukotriene- C4, Leukotriene- D4, Leukotriene-E4
***STRONGEST VASODILATORS OF THE HUMAN BODY
What are the diseases associated with Type I hypersensitivity reactions?
Localized Type I Hypersensitivity Reactions:
Allergic Reactions, Rhinitis, Angioedema, Hay Fever
Granulized Type I Hypersensitivity Reactions:
Anaphylactic Shock
What is the key differentiating factor for Type 2 Hypersensitivity Reactions?
Antigen is always fixed and intrinsic to the tissue in which reaction occurs (IgG and IgM: “General Motors” Ab)
No free immune complexes
What are some of the common diseases associated with Type 2 Hypersensitivity reactions?
Acute Rheumatic Fever, Glomerulonephritis, Myasthenia Gravis, Hyperthyroidism (Grave’s Disease), Hemolytic Anemia
Mechanisms for these Type 2 Hypersensitivity Reactions?
Grave’s Disease/ Hyperthyroidism–> Ab binding to the TSH receptors will cause an increase in T3, T4 which will cause adaptive immune cells to attack and destroy these cells
Myasthenia Gravis–> attack of the immune cells by binding of Ab to the muscle receptors causing them to be the site of degradation!
Glomerulonephritis–> binding of complement antigens to the receptors of the glomerulus basement membrane makes these cells susceptible to cell-mediated attack.
Acute Rheumatic Fever–> streptococcus looks similar to certain protein on the heart which causes these receptors to start being degraded by immune cells as a response.
What are the 2 types of Type 3 Hypersensitivity reactions?
Immune Complex Formation: Generalized & Localized
Generalized (Serum Sickness)
Localized (Arthus Reactions)
What is the general process for Type 3 Hypersensitivity reactions?
It is dependent on the complement system:
Ab binds to Ab-antigen creating immuno-complex; this immunocomplex cannot be broken because macrophage activity is absent.
The Results:
The immune complex that is left behind will be activated by complement proteins which will settle in the walls of blood vessels.
- Formation of the Ag-Ab Complex
- Complement Activation
- Local necrotic Cells attack into the blood vessels
What is the localized arthrus reaction for Type 3 Hypersensitivity reactions?
Type 3 hypersensitivity reaction
-characterized by localized inflammation; fever, fatigability, general lymphadenopathy, raised under the skin
What are some other examples of Type 3 Hypersensitivity reactions?
Systemic Lupus Erythrematosus Serum Sickness (General) Arthus Reaction (Local) PolyARTERITIS Nodosa Post-Streptococcal Glomerulonephritis Farmer's Lung
What are Type IV Hypersensitivity Reactions?
Delayed Type Hypersensitivity Reactions:
- TH1 Cells are primarily activated
- Tuberculoid Test (Tuberculosis)
- Granuloma formation (inside epithelial cells + outside= macrophages)
Delayed Type Hypersensitivity Reactions:
Macrophage engulfment–> presentation to Th cell via IL-12–> Proliferation of many Th1 Cells (secretion of IL-2) –>clonal expansion–> Mature Th1 Cell secretion of TNF-GAMMA + IFN-GAMMA (Type 2 Interferon)
Mass migration of phagocytes to the site of infection*** to create granules around the epithelia
TNF–> increase the adhesion molecules for receptors
IFN-gamma–> recruitment of macrophages
What are examples of Type 4 Delayed Onset Hypersensitivity Reactions?
- Urschiol Oil for Poison Ivy (Dermatitis)
- TB Reaction
- Multiple Sclerosis
- Diabetes Mellitus I (TH1 cell mediated, Glutamic Acid Decarboxylase Enzyme Destruction on Insulin Receptors)