Hypersensitivity Flashcards
How are hypersensitivity reactions able to arise?
- uncontrolled responses to foreign Ags
2. Autoimmune responses against self Ags
Describe Type 1 hypersensitivity
Immediate; caused by the release of mediators from mast cells (histamine, proteases, prostaglandins, leukotrienes, and cytokines)
-response to Environment in an allergic response (Th2)
Define atopy
tendency to develop allergies
Describe the primary encounter with the allergen (initial)
Allergen is inhaled, ingested, injected or contacted
B cells pick up the allergen and take it to the T cells, where they are formed into IgE secreting plasma cells
This IgE that is formed goes and binds to FcERI on the surface of mast cells waiting for the next exposure
Describe the subsequent allergen exposure (second) and what happens
allergen comes in contact with the mast cells who freak out and release all of the mediators resulting in vascular and smooth muscle contraction (vasoactive amines, prostaglandins, leukotrienes, and histamine), Endothelial vasodilation (histamine, prostaglandins), and leukocyte and chemotaxis activation (cytokines)
Differentiate between the immediate and late phases of a response to an allergen
Immediate:
-vascular and smooth muscle; vasodilation, congestion and edema
Late:
-inflammatory infiltrate of eosinophils, neutrophils, and T cells
Describe asthma
Reversible airway obstruction that is caused by an allergen- causes an inflammatory response including
increased capillary permeability, spasmodic contraction of smooth muscle around the bronchi (leading to SOB)
Describe anaphylaxis
exposure to an allergen causes a massive release of vasoactive amines and cytokines leading to extreme smooth muscle contraction and vasodilation
This leads to blood pressure drop and vascular shock
smooth muscle contraction leads to the contraction of the airway muscles, which makes breathing difficult
Describe allergen testing
tests type 1 hypersensitivities on the arm or the back with standardized allergens that are injected into the dermis; positive reactions result in redness and swelling
What are the aims of Allergen-SIT?
- induce T cell tolerance
- increase the thresholds for mast cell and basophil activation
- decrease IgE mediated histamine release
To generate FOXP3+CD4+CD@%_ Treg cells
Describe Type II Hypersensitivity
Disease caused by Abs to Cell or tissue Ags which causes local inflammation
- IgG and IgM activate the CP of the complement, which leads to increased C3a and C5a, leading to inflammation
- Abs go to the FcRy or CR1 receptors which lead to the increase of the release of ROS and lysosomal enzymes, which will cause inflammation to the tissues
How are Abs able to cause diseases such as
- Graves disease
- Myasthenia graves
- Abs stimulate the activity of the thyroid stimulating hormone receptors causing hyperthyroidism
- Abs inhibit ACH from binding to the receptor
Describe a penicillin induced anemia
drug binds to the erythrocyte surface and induces and anti-drug Ab
improves when the drug is stopped
Describe a quinidine induced anemia
autoAbs form complexes with the drug
immune complexes can bind to the surface through CR1
treatment: immunosuppression and plasmaohoresis to remove the complexes
Describe a methyldopa induced anemia
Induces and anti-drug Ab that cross react with an rh antigen
treatment: immunosuppression and plasmapharesis
What are the type 2 hypersensitivity diseases?
- autoimmune hemolytic anemia
- Autoimmune thrombocytopenia purpuratus
- Goodpastures syndrome
- myasthenia gravis
- pemphigus vulgaris
- pernicious anemia
- rheumatic fever
Describe Type III Sensitivity
Diseases mediated by immune complexes of circulating antigens and IgM or IgG Abs that are deposited in I the vascular basement membrane
Ab-Ag immune complexes may be formed in circulation and deposited in blood vessels, kidneys, or lungs; major mechanism triggering tissue damage is the CP of complement activation and recruitment of leukocytes
What are the diseases of Type III Hypersensitivity?
- SLE
- Polyarteritis nodosa
- Post-streptococcal glomerulonephritis
- Serum sickness (clinical and experimental)
- Arthus reaction (experimental)
Describe Type IV Hypersensitivity
Diseases mediated by T cells; CD4+ are cytokine mediated inflammation and CD8+ are T cell-mediated cytolysis; major triggers are autoimmunity, exaggerated or persistent responses to environmental Ags and some microbial Ags; tissue injury is caused by inflammation induced by cytokines, mainly Th1 and Th17 cells, macrophages, and/or killing of host cells by CD8+ CTLs
What are the diseases of Type IV Hypersensitivity?
- Multiple Sclerosis
- Rheumatoid Arthritis
- Type 1 (insulin-dependent) Diabetes Mellitus
- Crohn’s Disease
- Contact hypersensitivity (poison ivy reaction)
- Chronic infections (tuberculosis)
Describe Delayed-Type Hypersensitivity
Injurious cytokine-mediated inflammatory reaction resulting from activation of CD4+ T cells; develops 24-48 hrs after Ag exposure; may be sensitized for DTH reactions by microbial infection (TB) or by contact sensitization with poison ivy, metals, or some chemicals
***PPD (protein Ag of mycobacterium tuberculosis) elicits a DTH reaction, called the tuberculin reaction
Explain Allergic Contact Dermatitis (ACD)
Caused by environmental exposure to external Ags that in contact with the skin trigger inflammatory reaction; results from a DTH reaction; metals are most common Ags
- Sensitization to metals can occur at any age, even in neonates
- Costume jewelry, particularly earrings, is linked to increased sensitization to nickel and cobalt
- most common source of sensitization to chromium is leather
