Immunology - Block 3 - Part 2

davidwurbel7's version from 2015-11-28 03:10


Question Answer
Over reaction of the IS, resulting in tissue injury and diseaseHypersensitivity
Ag cross-links IgE on mast cells, triggering release of mediators. First and FastImmediate 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 leukocytesImmune Complex-Mediated Hypersensitivity (Type III)
Cytokine-mediated inflammation (T cell induced)T Cell-Mediated Hypersensitivity (Type IV)
A rapid, IgE antibody and mast cell-mediated vascular and smooth muscle reaction, often followed by inflammationType I Hypersensitivity
Asthma, food allergies, local wheal and flare, and anaphylactic shockType I Hypersensitivity
Individuals with a strong propensity to develop allergic reactions (ie family history of allergy)Atopy
Production of IgE antibodies. Binding of IgE to Fc receptorsFirst exposure to allergen
Cross-linking of the previously bound IgE. Release of mast cell mediatorsSubsequent Exposure to Allergen
When some individuals encounter antigens, the dominant T cell response is the development of TH2 cellsAllergy
Class switching leads to secretion of IgE which binds to FcεRI onMast Cells
The antigens are presented to CD4 T cells, stimulating a TH2 responseIL-4
Release of granule containing histamineMast Cell Degranulation
Characteristics of chronic allergic inflammationEosinophils
This chemical released by TH2 cells stimulate the bone marrow to increase the production of eosinophils and basophilsIL-5
Mast-cell degranulation initiates the inflammatory response, which induce eosinophils to expressFcεRI
IgE binds to this receptor on the mast-cells with the initial exposure to an antigen in Type I HSFcεRI
This actually will activate eosinophilsAllergen
IL-5 released by TH2 cells also stimulate the bone marrow to produceEosinophil and Basophils
Released histamine and other mediators cause increased permeability of blood vessels, immediate local reactions can last for up to 30 minutesImmediate Reaction
A more widespread swelling inflammation due to the cytokines, chemokines & leukotrienes by activated mast cells and eosinophilsLate-Phase Reaction
Immediate reaction is due to release of this chemicalHistamine
Late-phase reaction is due to release of theseCytokines, Chemokines and Leukotrienes
Molecules released by mast cells that are toxic to parasites, increase vascular permeability and cause smooth muscle contractionHistamine and Heparin
Molecules released by mast cells that promotes inflammation, stimulates cytokine production by many cell types and activates endotheliumTNF-α
Molecules released by mast cells that stimulate and amplify Th-2 cell responseIL-4 and IL-13
Molecules released by mast cells that promote eosinophil production and activationIL-4 and IL-5
Molecules released by mast cells that cause smooth muscle contraction, increase vascular permeability and cause mucus secretionLeukotrienes
An amine derivative of the amino acid histidineHistamine
Acute allergic reactions involve histamine binding to this receptor on smooth muscle cells and on endothelial cells of blood vesselsH1 Receptor
Allergens in the blood and activate mast cells throughout the body, which increase in vascular permeability and a widespread relaxation of smooth muscleType I: Systemic Anaphylaxis
Fluid leaving the blood causes the blood pressure to drop drastically, a conditionAnaphylactic Shock
Treatment that increases the blood pressure and reverse airways obstruction and be life-saving in anaphylaxisEpinephrine
Most common cause of systemic anaphylaxis is allergy to thisPenicillin
The characteristic immediate reaction to an injected allergen in a skin test or insect bite, in which an irregular blanched swelling appears, surrounded by an area of rednessWheal and Flare
Allergens are inhaled and enter the mucosal tissue. Pre-sensitized mast cells release mediators, triggering swelling, activation of eosinophils, eventually resulting in mucus productionType I: Allergic Rhinitis (Hayfever)
Allergens are inhaled and enter the mucosal tissue. Histamine produced by mast cells triggers smooth muscle contractionType I: Allergic Asthma
Associated with activated Th2 cells and high influx of eosinophils, develops into a Type IV HypersensitivityChronic Asthma
Ingested antigens can trigger severe systemic anaphylaxis from the mediators release by mucosal mast cellsType I: Food Allergies
Used to treat anaphylaxis. Causes vascular smooth muscle contration and increases cardiac output, relaxes airway muscle and inhibits mast cell degranulationEpinephrine
Used to treat bronchial asthma. Reduces inflammationCorticosteroids
Relax bronchial smooth muscle and reduce inflammationLeukotriene Antagonist
Generally use to block the actions of histamine on vessels and smooth muscleAntihistamines
Autoantibodies that directly bind to self antigen on specific cells, which triggers tissue damage via complement of PMNsType II Hypersensitivity Reactions
Antibodies may modify the function of cells by binding onto receptors that cause disease by stimulating or blocking receptor functionType II Hypersensitivity Reactions
Antibodies IgG bound to host cells initiate immune response triggersADCC
Antibodies IgG and IgM bound to host cells initiate immune response triggersComplement
Complement activatesPMNs
When tissue is coated with antibodies, the complement cascade overwhelms the complement inhibitors, leading to C3b deposition on host tissueComplement Activation
PMNs become “frustrated” and release these due to the inability to phagocytosis antibody bound cellReactive Oxygen Species (ROS)
Antibodies may cause pathology by interfering with this, such as hormone receptor signalingCellular Functions
If a Rh-negative woman carries a Rh-positive fetus, she will produce Rh-antibodies for the second pregnacny. This condition may occur in the fetus/newbornHemolytic Disease of the Newborn
This should be given to Rh-negative women to prevent sensitization (28 week of gestation and within 72 hours of delivery)Anti-D Polyclonal Antibodies (Rogham)
Small molecule that can elicit an immune response only when attached to a large carrier such as a proteinHapten
What is the cell type that has the carrier protein for penicillinErythrocytes
In pernicious anemia, the antibodies are against thisIntrinsic Factor
Intrinsic factor binds this in the stomachB12
ABO blood group immune interaction is this type of reactionType II Hypersensitivity
In this disease, antibodies target erythrocyte membrane proteinsAutoimmune Hemolytic Anemia
In this disease, antibodies target platelet membrane proteinsAutoimmune Thrombocytopenic Purpura
In this disease, antibodies target proteins in the intercellular junctions of epidermal cellsPemphigus Vulgaris
In this disease. antibodies target type IV collagen in basement membranes of kidney glomeruli and lung alveoliGoodpasture's Syndrome
In this disease. antibodies target streptococcal cell wall antigen. The antibodies cross-react with myocardial antigenAcute Rheumatic Fever
In this disease. antibodies target acetylcholine receptorMyasthenia Gravis
In this disease. antibodies target TSH receptorGraves' Disease
In this disease. antibodies target Intrinsic factor of gastric parietal cellsPernicious Anemia
Reactions are caused by tissue deposition of immune complexes formed from IgG and soluble antigensType III Hypersensitivity
Fix complement efficiently and are readily taken up by phagocytes via CR1, FcR and C3bR and removed from circulationLarge Immune Complex
Less efficient at fixing complement, they tend to circulate in the blood and become deposited in blood vessel wallsSmaller Immune Complex
Hypersensitivity reaction can be induced in the skin by subcutaneous injection of the antigen. Develops more slowly than the immediate Type I hypersensitivity reaction, but faster than the delayed type IV hypersensitivity reactionArthus Reaction
Arthus reaction shows signs and symptoms roughly this long after exposure12 - 24 Hours
Bacterial infections were treated by injecting patients with serum taken from horses that had been immunized with bacteria or their toxinsType III 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
Type III Serum Sickness shows signs and symptoms roughly this long after exposure24-48 Hours
Immune complexes are deposited in endothelial basement membrane of the kidney, usually 1-2 weeks post-infectionType III Post-Streptococcal Glomerulonephritis
The most common form of immune-complex glomerulonephritis worldwide; characterized by deposits of IgA on the glomeruli with unknown causeIgA Nephropathy
Clinical manifestations include nephritis, arthritis and vasculitis. Antibody complexes formed by antibodies binding to DNA, nucleoproteins and other proteinsSystemic Lupus Erythematosus
Clinical manifestation includes vasculitis. Antibody complexes formed by antibodies binding hepatitis B virus surface antigenPolyarteritis Nodosa
Clinical manifestation includes nephritis. Antibody complexes formed by antibodies binding streptococcal cell wall antigensPost-Streptococcal Glomerulonephritis
Clinical manifestation include systemic vasculitis. nephritis and arthritis. Antibody complexes formed by antibodies binding various foreign protein antigens usually in injectionsSerum Sickness
Clinical manifestation includes cutaneous vasculitis. Antibody complexes formed by antibodies binding various protein antigensArthus Reaction
Reactions are mediated by antigen-specific CD4+ T cells that release cytokines and activate macrophagesType IV Delayed Hypersensitivity
Reactions taking place 48 - 72 hours after exposure to antigenType IV Delayed Hypersensitivity
Type IV hypersensitivity requires these cells being activated in the presence of antigenT-Cells
The delayed-type (type IV) hypersensitivity response is directed by chemokines and cytokines released byAntigen-Specific Th1 Cells
An example of Type IV hypersensitivity is this testTB Tuberculin
Pentadecacatechol penetrates the outer layers of the skin, penetrate inside the cytosol (antigenic peptides are presented by class I molecules to CD8 cells). Then CD8 T cells can cause tissue damage and also IFN-gamma is releasedType IV - Contact Dermatitis
Th1 Type IV hypersensitivity reaction to this protein of the wheat flourGliadin Peptide
Inflammation in the gut wall leading to atrophy of intestinal villi, mal-absorption of the nutrients and diarrheaCeliac Disease
Microbes produce toxin which binds to all MHCII and TCR complex, regardless of specificity of antigenType IV - Superantigen
Binding of this 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
T cells target pancreatic islet antigens. Genetic associations with PTPN22 and insulin. Manifests as impaired glucose metabolism and vascular diseaseDiabetes Mellitus Type I
T cells target unknown antigens in the joints. Genetic associations with PTPN22. Manifests as inflammation of synovium and erosion of cartilage and bone in jointsRheumatoid Arthritis
T cells target myelin protiens. Genetic associations with CD25. Manifests as demyelination of neuron in the central nervous system, sensory and motor dysfunctionMultiple Sclerosis
T cells target is unknown. Genetic associations with NOD2. Manifests as inflammation of the bowel wall; abdominal pain, diarrhea and hemorrhageInflammatory Bowel Disease
T cells target modified skin proteins. No Genetic associations. Manifests as delayed-type hypersensitivity reaction in skin; rashContact Sensitivity
T cells target microbial proteins. No Genetic associations. Manifests as chronic conditionsChronic Infections
T cells target virally encoded proteins. No Genetic associations. Manifests as CTL-mediated hepatocyte death, liver dysfunction; fibrosisViral Hepatitis
T cells target polyclonal antigens. No Genetic associations. Manifests as fever, shock, related to systemic inflammatory cytokine releaseSuperantigen Mediated Diseases (Toxic Shock Syndrome)

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