Hypersensitivity 2

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Hypersensitivity Types II-IV
Type II Cytotoxic Type III Immune Complex Type IV T Cell-Mediated (DTH)
Hypersensitivity II III(antibody mediated diseases)
Antibodies (other than IgE) may cause tissue injury diseases by binding directly to their target organs extracellular matrix (type II) or by forming immune complexes that deposit mainly in blood vessels (type III) .
Cytotoxic hypersensitivity
Characteristics of Cytotoxic Hypersensitivity
Antibodies directed against cell surface or tissue antigen Characterized by complement cascade activation and various effector cells
Complement Activated C3 forms opsonin recognized by phagocytes Formation of membrane attack complex (lytic enzymes Formation of chemotactic factors Effector cells possess Fc and complement receptors macrophages/monocytes neutrophils
Mechanisms of tissue injury
Examples of Type II Hypersensitivity
Hypersensitivities
Drug-induced cytotoxic reactions Some drug molecules bind larger molecules Stimulate the production of antibodies Can produce various diseases Immune thrombocytopenic purpura Agranulocytosis Hemolytic anemia
Drug-Induced ReactionsAdherence to Blood Components
complement
blood cell adsorbed drug or antigen drug metabolite
antibody to drug
lysis
Immune (Toxic )Complex Hypersensitivity (Type III)
Hypersensitivities
Diseases associated with immune complexes
Inflammatory Mechanisms in Type III
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Immune Complex Mediated Hypersensitivity
Disease Models
Serum sickness Arthus reaction
Arthus reaction Type-III
Weal flare reaction Type-I
Serum Sickness (contd)
Serum sickness
T-Cell Mediated Hypersensitivity(Type IV / Delayed-Type)
Manifestations of T-Cell Mediated Hypersensitivity
Allergic reactions to bacteria, viruses and fungi Contact dermatitis due to chemicals Rejection of tissue transplants
General Characteristics of DTH
Types of Delayed Hypersensitivity
Delayed Reaction maximal reaction time Contact 48-72 hours tuberculin 48-72 hours granulomatous at least 14 days
Contact Hypersensitivity
Contact dermatitis
Ag possibly enters sebaceous glands Lesions vary from macules papules to vesicles which subsequently breakdown leaving weeping surface typical of acute eczematous dermatitis. Detected by patch test
Contact dermatitis reaction
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Allergic Contact Dermatitis Response to Poison Ivy Hapten
Atopy Patch Tests
Atopy Patch Tests (APT) on the skin can detect delayed hypersensitivity reactions to foods, but are usually employed to identify triggercontact allergens such as nickel, rubber, dyesand cosmetics
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The food allergen is applied to the skin under an occlusive cover (called a Finn chamber) and the skin is assessed after 48 and 72 hours for a wheal reaction. Any redness or micro-blistering is then measured and graded as a positive reaction.
Tuberculin Hypersensitivity
Maximum at 48-72 hours Inflitration of lesion with mononuclear cells Responsible for lesions associated with bacterial allergy cavitation, caseation, general toxemia seen in TB May progress to granulomatous reaction in unresolved infection
Granulomatous Hypersensitivity
Granuloma in a leprosy patient
Examples of Microbial-Induced DTH
Viruses (destructive skin rashes) smallpox measles herpes simplex Fungi candidiasis dematomycosis coccidioidomycosis histoplasmosis Parasites (against enzymes from the eggs lodged in liver) leishmaniasis schistosomiasis
Type-IV
Type-III
Type-II
Type-I
characteristic
Comparison of hypersensitivity reactions
TB test, poison ivy, granuloma
pemphigus, Goodpasture
hay fever, asthma
examples
antibody
IgE
IgG, IgM
IgG, IgM
none
antigen
exogenous
cell surface
intracellular
soluble
response time
15-30 min.
Min.-hrs
3-8 hours
48-72 hours or longer
appearance
Weal flare
Lysis necrosis
Erythema edema
Erythema induration
baso- and eosinophils
Ab and complement
histology
PMN and complement
Monocytes lymphocytes
T-cells
antibody
antibody
antibody
transfer with
drug can bind to red blood cells, causing them to be recognized as different.B cell proliferation to produce IgG,IgM,bind to these antigens to form complexes that activate the classical pathway
Study Guide What is the difference between Type II and Type III
Study Guide What is the circulating equivalent of the Langerhans cell What is the carrier in hapten-induced eczema
Study Guide Are you familiar with tuberculosis