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Immuno Lec 7

Hypersensitivity I-IV

What is the one common denominator of all hypersensitivity reactions? The person must first be sensitized.
Hypersensitivity excessive or inappropriate immune response that is damaging to the host. Four types. 1-3 are Ab mediated. 4 is T cell mediated. Occur only for a sensitized individual is reexposed
Type I Hypersensitivity Immediate. Allergies. IgE.
How does a person become sensitized, first exposure. B cell activation. Ag carried to 2* lymph organ. TH2 cell comes in contact. B cell binds antigen. TH2 recognizes epitope. Expresses Cd40L and IL-4. First exposure, Secretes IgM and IgD.
How does a person become sensitized, second exposure. Subsequent exposure, TH2 secretes IL4 and IL-13. Class switching to IgE. IgE moves to mast cell, binds via FCregion to mast cell in submucosa.Once IgE is sent to mast cells, person is sensitized.
What triggers Mast Cell Degranulation Cross-linking IgE on Mast Cell Surface. Multivalent antigens cause crosslinking which results in release of granular contents.
What is located in mast cell granules Histamine and serotonin. Increase vascular permeability and blood flow.
What happens after Mast Cell Degranulation The cell will recharge. It will rebind IgE. Since it binds IgE through FC region, no specificity.
Specificity of a mast cell On any mast cell, you can have IgE but specificity for various allergans because Mast cell binds via FC region to the IgE.
Immediate Reaction in Type I Hypersensitivity. Degranulation occurs, preformed meiators released, histamine, serotonin, neutrophil and eosinophil chemotactic factor. immediately cause vasodilation, SM contraction, increased mucus. IMMEDIATE REACTION.
What is key in initiating second phase of type 1 hypersensitivity? Neutrophil/eosinophil chemotactic factor.
Late Phase Reaction in Type 1 Hypersensitivity 8-10 hrs later. Il-5 causes activation, differentiation, survival of eosinophils, resulting in release of toxic granular proteins that damage tissue and we begin metabolizing lipid membrane on mast cells, producing leukotrienes and prostaglandins.
Immediate Reaction clinical appearance Wheal and Flare Reaction. Wheal = Raised fluid filled. flaire is redness. flare surrounds wheal. from histamine. appears within 30 min. due to a subcutanous local skin rxn. most benign.
Late reaction clinical appearance difuse lesion. widespread, edematous. Sustained for upwards of 8 hours due to late phase reaction.
Intravenous dosing of allergan Results in systemic absoprtion. Anaphlyaxis. degranulate mast cells body wide. most severe type 1.peripheral vasodilation. constriction of SM in bronchioles.
Clinical presentation of systemic anaphylaxis urticaria, wheezing, angioedema, vomiting, dyspnea
Intraderm skin test Wheal and flare. A positive test has a wheel and a flare, not just a wheel.
Inhalation of allergans results in Allergic rhinitis - nasal mucosa, conjuctiva, upper airways. Asthma - lower airways
Allergic Asthma Not just mast cell degranulation, also mucus build up. Effect of mediators on bronchiole lumen. Goblet cells increasing mucus as well.
Desensitization Desensitization. IgG and IgA blocking antibodies. produce IgG and IgA so they compete with IgE for allergan. IgG and IgA would opsonize the allergan before IgE could act. can be natural if you outgrow allergies, or can be induced by injection of antigen
Competition Strategies Administer FCepsilon region. No Fab. Binds to the mast cells. do not degranulate them.
pharmacologic clinical intervention antihistamines, chromolyn sodium prevents mast cell degranulation. corticosteroids prevent phospholipase C(first step in lipid membrane metabolism), epinephrine relax SM and increase HR to counteract initial effect
Type II Hypersensitivity Reaction IgG or IgM. Ab against cell structures. results in death by complement, opsonization, ADCC. examples: ABO antigen and Rh antigen
ABO blood group All RBC similiar structure H chain. if they have GalNac - A. If they have Gal - B. If neither - O. genotype encodes transferases that add GalNac or Gal to H Chain.
Type II Hypersensitivity Reaction results in Agglutination. Clumping of RBC that occurs when Ab binds RBC antigen and you cross link RBC.
Transfusion Reactions with mismatched blood Cells become coated with IgM and are destroyed via complement, ADCC, opsonization.
RhD blood group Rhesis. D antigen. Dominant Inheritance. No naturally occuring IsoHemmaglutinin. Only Matters when Rh- mother has a Rh+ child.
Hemolytic Disease of Newborns RhD- pregnant with RhD+ baby, Fetal blood mixes at time of delivery. Fetal RBC enters.IgM is 1st Ab produced,cant mount cytotoxic reaction,IgM doesnt cross placenta.2nd exposure to RhD, class switch, produce IgG, cross placenta, opsonization of fetal RBC.
When does sensitization of the mother occur in hemolytic disease of the Newborn Sensitization occurs after the first pregnancy. She has created IgM Abs to the D Antigen.
What occurs during second pregnancy with an RhD+ newborn? The IgM will undergo class switching during pregnancy to IgG. This can cross the placenta and attack the fetal RBC.
Treatment of Hemolytic disease of the Newborn Rhogam prevents sensitization. it is a blocking antibody. It is passive. You are giving IgG antiD antibodies. that bind to RhD+ fetal RBCs that come into maternal circulation. Given at 28 weeks and at delivery.
Direct Coombs test You test Fetal RBC directly to see if they have maternal antibody bound in order to assess. Then you add Anti-IgG, which triggers cross linking and agglutination. Anti-IgG binds to the FC region of Maternal IgG.
Indirect Coombs Test If you don't want to risk isolating the fetal RBC. taking maternal blood, seeing if mom has IgG that can bind to RhD+ antigen. only testing mom. if she does have AntiRhD Abs, you will see agglutination. Not absolutely sure that IgG has crossed placenta.
Type III Hypersensitivity Reaction Immune Complex. IgG or IgM. Ab forms with soluble Ag to form Ab/Ag complexes. Locally, called arthus reaction. Systemic - Serum Sickness
Arthus Reaction Form immune complexes that activate complement. form at zone of equivalences. Ab move away from BV, Ag towards. C3a and C5a increase vascular permeability, cause edema.also influx of neutrophils/platelets leads to tissue damage
Farmers Lung pulmonary reaction against mold spores, type 3
elephantiasis abs form complexes with antigens shed from filarial worms present in lymphatics. type 3.
Serum Sickness injection of large quantities of foreign antigen. Type 3. Passive immunization, you risk eliciting this. Helps immediately, but now person processes Ab and it is a foreign antigen. foreign Ag decreases, Ab increases to Ag. 7-12 days, symptoms and ZoE.
Serum Sickness outline deposition of circulating immune complexes. BM kidneys - glomerulonephritis BM joints - arthritis Skin - urticaria Symptoms 1-2 weeks following foreign protein/Drug. common mechanism in autoimmunity.
Type IV hypersensitivity Delayed Type. T cell dependent, CD4+. Activating macrophages, producing free radicals, cause localized tissue destruction, eliminate intracellular pathogens but also damage. Macrophages Key Cell Type.
Mediators in Type IV Hypersensitivity IFN-y - macrophage activation TNF-B - tissue destruction Monocyte/macrophage chemotactic factor. Done by TH1.
Mechanism of Type IV Hypersensitivity Must be prior sensitized. After 1-3 Days, TH1 cell activation and cytokine release. recruit T cells, macrophages, fluids. Predominantly macrophage infiltrate(T cells) and may have granuloma filtration. Langerhan Cells process it locally.
Contact Dermatitis Type IV. Ag=hapten. penetrate skin, covalently couple with host proteins. Langerhan Cells. now you have host carrier complex in body. processed by MHC. activates T cells. Patch testing used for this.
Created by: nady