Immunology Block III

ptheodore's version from 2015-11-07 15:06


Question Answer
Over reaction of the immune system, result into tissue injury and diseaseHypersensitivity
Ag cross-links IgE on mast cells, Triggering release of mediators, First and Fast (minutes)Immediate Hypersensitivity (Type I)
Abs (IgM and IgG) bind to Ag on human cells or tissues, leading to lysis (by complement) or phagocytosisAntibody-mediated Hypersensitivity (Type II)
Ag-Ab complexes activate complement, which attracts leukocytes. Three things (ABC) stuck together, Ag-Ab-ComplementAg-Ab complexes activate complement, which attracts leukocytes, Three things (ABC) stuck together, Ag-Ab-Complement
T cell-mediated Hypersensitivity (Type IV)Cytokine-mediated inflammation (T cell induced), 4th and last-delayed
A rapid, IgE antibody and mast cell-mediated vascular and smooth muscle reaction, often followed by inflammationType I hypersensitivity (Allergy)
asthma, food allergies, local wheal and flare, and anaphylactic shock are common types of which type hypersensitivityType I
Production of IgE antibodies, Binding of IgE to Fc receptors (mast cells)First exposure to allergen
Cross-linking of the bound IgE, Release of mast cell mediatorsRepeat exposure to allergen
The process of coating mast cells with IgE is calledSensitization
Binds to a high affinity Fce receptor, called, FceRIIgE
Synthesis & secretion of lipid mediators such as Prostoglandins/LeukotrienesLate Phase Response
Degranulation (release of granule containing histamine) is part of which IgE-mediated mast cell activationImmediate Response
Initial exposure to an allergen during IgE-mediated mast cell activationIncreases IgE
Mast cell degranulation and activation of TH2 cells cause the accumulation of act eosinophils at the siteIn allergic reaction
Eosinophils do not express FceRI, do not bind to IgE, and cannot therefore be induced to degranulate by antigenIn resting state
Released by TH2 cells stimulate the bone marrow to increase the production of eosinophilsIL-5
Released by TH2 cells also stimulate the bone marrow to produce basophilsIL-5
Recruited into sites of allergic reactions, where they are activated to degranulate by antigen crosslinking the IgE bound to the FceRI on the basophil cell surfaceEosinophils & Basophils
Primary molecule released by mast cells during allergic reactionHistamine
Secondary molecule released by mast cells during an allergic reactionLeukotriene
Remodeling of connective tissue matrixTryptase, chymase, cathepsin G & Carboxypeptidase
Toxic to parasites, increase vascular permeability & cause smooth muscle contraction (immediate response)Histamine & Heparin
Promotes inflammation, stimulates cytokines production by many cell types, activates endothelium (late response)TNF-alpha
Stimulate & amplify Th-2 cell responseIL-4 & IL-13
Promote eosinophil production & activationIL-3, IL-5, GM-CSF
Chemotactic for monocytes, macrophages & neutrophilsCCL3
Cause smooth muscle contraction, increase vascular permeability, cause mucus recreationLeukotrienes C4, D4 & E4
an amine derivative of the amino acid histidineHistamine
Acute allergic reactions involve histamine binding to the H1 receptor on smooth muscle cells and on endothelial cells of blood vessels
Individual who is prone to allergic responsesAtopic
An increase the blood pressure and reverse airways obstruction and be life-saving in anaphylaxisEpinephrine
The characteristic immediate reaction to an injected allergen in a skin test or insect bite, in which an irregular blanched wheal appears, surrounded by an area of redness Wheal & Flare
is associated with activated Th2 cells and high influx of eosinophils, develops into a Type IV HypersensitivityChronic Asthma
Produced by mast cells triggers smooth muscle contractionHistamine
Fluid leaving the blood causes the blood pressure to drop drastically, a condition calledanaphylactic shock
Caused by allergens in the blood and activate mast cells and complement throughout the body, which increase in vascular permeability and a widespread constriction of smooth muscleType I Systemic anaphylaxis
Can increase the blood pressure and reverse airways obstruction and be life-saving in anaphylaxisEpinephrine
The most common cause of systemic anaphylaxis is allergy to Penicillin
localized raised itchy swelling in the skinUrticaria
diffuse swelling due to activation of mast cells in deeper subcut tissueAngioedema
What is the therapy of choice for AnaphylaxisEpinephrines
What is the mechanism of action of epinephrine for anaphylaxisCauses vascular smooth muscle contraction & increases cardiac output, relaxes airway muscle, inhibits mast cell degradation
What is the therapy of choice for bronchial asthmaCorticosteroids & Leukotriene antagonists
What the mechanism of action of Leukotriene antagonists for bronchial asthmaRelax bronchial smooth muscle & reduce inflammation
What it is the mechanism of action of Corticosteroids for bronchial asthmaReduce inflammation
What is the mechanism of action of antihistamines?Block actions of histamine on vessels and smooth muscles
Inhibits effects of mediators on specific receptors & target mediator actionantihistamines & beta-blockers
Drugs use to treat general anti-inflammatory effects & they target chronic inflammation reactionsCorticosteroids
Antibodies bound to host cells initiate immune response in type II hypersensitivityIgG triggers ADCC, IgG & IgM triggers complement & complement activates PMNs
The antibodies are most often autoantibodies that directly bind to self antigen on specific cells, which triggers tissue damage via complement of PMNs Type II hypersensitivity reaction
Antibodies may modify the function of cells by binding onto receptors that cause disease by stimulating or blocking receptor functionType II hypersensitivity reaction
IgG on tissue is a “docking site” C1r-q, which triggers complement in which type of hypersensitivityType II hypersensitivity
During mechanism of type II hypersensitivity PMNs become “frustrated” and release toxic molecules ROS
is a small molecule that can elicit an immune response only when attached to a large carrier such as a protein Hapten
Antibody target equal Penicillin plus RBC antigen & Consequence is AnemiaType II (Drug-Induced Hemolytic Anemia)
Antibody target is equal Intrinsic Factor or Parietal cell, Both are responsible for Vitamin B12 uptake & Consequence is Anemia Type II (Pernicious Anemia)
Caused by tissue deposition of immune complexes formed from IgG and soluble antigens Type III Hypersensitivity reaction
Develops more slowly than the immediate Type I hypersensitivity reaction, but faster than the delayed type IV hypersensitivity reactionType III Arthus reaction
Can be induced in the skin by subcutaneous injection of the antigenType III hypersensitivity reaction
Historically, bacterial infections were treated by injecting patients with serum taken from horses that had been immunized with bacteria or their toxins, which triggeredType III Hypersensitivity serum sickness
Most often happens as a result of the use of mouse monoclonal antibodies or drug to treat cancer or autoimmune diseaseType III Serum sickness
Most common form of immune-complex glomerulonephritis worldwide; characterized by deposits of IgA on the glomeruli with unknown causeIgA nephropathy
Are mediated by antigen-specific CD4+ T cells that release cytokines and activate macrophagesType IV hypersensitivity reactions
Is directed by chemokines and cytokines released by antigen-specific Th1 cellsdelayed-type (type IV) hypersensitivity response
Th1 reaction to the gluten protein (gliadin peptide) of the wheat flourType IV Celiac disease
Strong co-relation with HLA-DQ2 or DQ8Type IV Celiac disease
Its binding causes NON-SPECIFIC activation of T cells and release of excess pro-inflammatory cytokinesSuperantigen
T cells of the recipient react against the MHC of the donor APCAcute graft rejection
T cells from the recipient react against the peptides (donor MHC peptide) presented by recipient APCChronic graft rejection

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