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Immunology chapter-11


By: Marudhapriya (88 month(s) ago)

Elaborate presentation! useful to students.

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Hypersensitivity : 

Hypersensitivity Lecturer: Xu Lin

Introduction : 

Introduction What is hypersensitivity? It is excessive immune response which leads to undesirable consequences, i.e. tissue or organ damage/ dysfunction. Type: type?, ?, ?, ? hypersensitivity Ab mediated: type?, ?, ? T-cell mediated: type ?

Type ? hypersensitivity : 

Type ? hypersensitivity IgE mediated, immediate hypersensitivity/ allergy Major features: React and disappear quickly on re-exposure to Ag Dysfunction rather than severe tissue and cell damage occurs Obvious individual difference and genetic correlation

Component and cells : 

Component and cells Allergen: An antigen that causes allergy. Hapten can turn into allergen by carrier effect (hapten +carrier ?immunogen) Common allergen: inhalant allergen (grass pollen, animal dander, feces from mites in house dust, etc.), some kinds of food and drugs

Reaginic antibody (IgE) : 

Reaginic antibody (IgE) The main anaphylactic Ab in human IgE can bind FceR?on mast cells and basophils by its CH4 domain, cause anaphylaxis

Mast cells : 

Mast cells Express high affinity IgE Fc receptor FceR?, granules contain mediators. Distribution: connective tissues, mucosa, skin Anaphylaxis is triggered by clustering of IgE receptors (FceR?) on mast cells and basophils through cross-linking

IgE-binding Fc recepors : 

IgE-binding Fc recepors FceR?: high affinity receptor of IgE on mast cell/ basophil, activate mast cell/ basophil FceR?:low affinity

Mediators released by mast cells : 

Mediators released by mast cells Primary mediators (preformed): heparin, histamine, neutral protease, eo-sinophil & neutrophil chemotactic factors, provoke early phase(immediate) reaction Secondary mediators(newly synthesi-zed) : leukotrienes(LTB4, LTC4 and LTD4), PGD2, PAF, CKs(IL-4, GM-CSF), induce late phase reaction

Mechanism of type?hypersensitivity : 

Mechanism of type?hypersensitivity Allergen?host?specific B-cell?IgE?Fc fragment of IgE binding FceR?on mast cells/ basophils Allergen once again enter the host ?binding IgE ?cross-linking of IgE ? cross-linking of FceR?? mast cell activation? degranulation? mediators release? anaphylaxis symptoms

Slide 10: 

Early phase response: short-lived, resolve within 1 hr. Increase of vasopermeability, smooth muscle contraction, gland hypersecretion and vasodilation Late phase response: inflammation, peak at around 5 hrs, last for several days. Eosinophils, mast cells, basophils, T-cells and neutrophils infiltration.

Slide 11: 

The mechanism of type?hypersensitivity

Typical diseases of anaphylaxis : 

Typical diseases of anaphylaxis Systemic anaphylaxis(anaphylactic shock): fatal, venom from bee, wasp; drugs such as penicillin, antitoxins, etc. Localized anaphylaxis(atopy): the tend-ency to manifest localized anaphylaxis is inherited and called atopy. typical diseases: asthma, hayfever, eczema, food allergy, etc.

Atopy : 

Atopy Allergic rhinitis: Hay fever, airborn allergens, symptoms include shedding tears, sneezing, coughing, etc. Asthma: airborn/blood-born allergens. Occur in lower respiratory tract Cardinal clinic and physiological features: variable airflow obstruction, bronchial hyper-responsiveness.

Slide 14: 

Food allergies: diarrhea, vomiting, wheal and flare reaction Atopic dermatitis: eczema, urticaria. itch, desquamation, pachyderma

Therapy of type?hypersensitivity : 

Therapy of type?hypersensitivity Allergen avoidance: best if possible, but often impractical. Skin test Hyposensitivity: repeated injection of increasing doses of allergen. Allergic rhinitis Drug: antihistamines; epinephrine (also called adrenaline), etc. Immediate injection of adrenaline could rescue anaphylactic shock

Slide 17: 

Atopic allergies and their treatment

Type ? hypersensitivity : 

Mediated by IgG and/or IgM Mechanism: Ag present on the surface of cells? im-munity activation?Ab?tissue damage/ dysfunction Tissue damage caused by: Opsonic adherence: phagocytosis Complement: membrane damage ADCC: cell destruction Type ? hypersensitivity

Slide 19: 

Mechanism of tissue damage of type? hypersensitivity

Type ? associated diseases : 

Type ? associated diseases Transfusion reaction: mismatched blood transfusion cause complement-mediated hemolysis. ABO blood group: isohemagglutinins(IgM) Prevention: cross-matching between donor and recipient blood

Heamolytic diseases of newborn : 

Heamolytic diseases of newborn Rh incompatibility: Rh blood groups Rh- mother has the first Rh+ baby? mother sensitized by baby’s erythrocy-tes ?anti-Rh IgG Mother has the second Rh+ baby? IgG enter the fetus through placenta? destruction of fetal RBC

Slide 22: 

Hemolytic disease of the newborn due to rhesus incompatibility

Drug-induced hemolytic anemia : 

Drug-induced hemolytic anemia Drug adsorb RBC proteins?Anti-RBC IgG/IgM?complement, opsonization, ADCC ?RBC lysis, anemia

Grave’s disease and myasthenia gravis : 

Grave’s disease and myasthenia gravis Special class of type ? hypersensitivity, Autoimmune diseases, tissue/organ dysfunction Grave’s disease: anti-TSH receptor Myasthenia gravis: anti-acetylcholine receptors

Slide 25: 

Myasthenia gravis Grave’s disease

Type ? hypersensitivity : 

Type ? hypersensitivity Participate by IgG/IgM, induced by de-position of immune complex (IC) Formation of IC: Excess of antigen over a protracted period Deposition frequently observed: blood-vessel walls, synovial membrane of joints, glomerular basement of kidney

Slide 27: 

Mechanism of type ? hypersensitivity

Slide 28: 

Tissue damage caused by: Complement activation and attraction of neu-trophils: release tissue damaging mediators Stimulation of Mf: release proinflammatory cytokines Aggregation of plate-lets: cause microthrombi and vasoactive amine release

Slide 29: 

Immune complex-mediated (type ?) hypersensitivity

Type ? associated diseases : 

Type ? associated diseases Localized type ? reaction: the Arthus reaction, erythematous and edematous, intense neutrophil infiltration Generalized type ? reaction: Serum sickness: injection of foreign protein (horse serum) SLE: systemic lupus erythematosus, DNA/ anti-DNA/ complement

Type ? associated diseases : 

Rheumatoid arthritis: rheumatoid factor (RF): anti-IgG autoantibodies, usually IgM. IgM-IgG complex deposit in joints Immune complex glomerulonephritis: Ag-Ab-C3 deposit glomerular basement membrane Others: drug reactions, infectious diseases Type ? associated diseases

Type ? hypersensitivity : 

Type ? hypersensitivity Delayed-type(DTH), T-cell mediated, 24-72 hr after Ag contact, Ab not involve Results from excessive CMI, secondary response, chronic granuloma Mechanism: CD4+Th1: Tm?Ag:MHC??effector T-cell?MCP-1, IFN-?, TNF, IL-2?Mf attraction and activation?tissue damage

Immune pathogenesis : 

Immune pathogenesis CD8+CTL: primed CTL?Ag:MHC?? perforin/ Fas-FasL?target cell death

Type ? associated diseases : 

Insulin-dependent diabetes mellitus (IDDM): insulin-producing ßcells Multiple sclerosis(MS): central nervous system, myelin Ag Contact dermatitis: foreign low molecular weight materials, hapten-carrier, topical Infectious diseases: tuberculosis Others: hashimoto’s thyroiditis, IBD Type ? associated diseases

Summary : 

Summary Hypersensitivity is excessive immune response which leads to undesirable consequences, i.e. tissue or organ damage/ dysfunction. Type: type?, ?, ?, ? hypersensitivity Ab mediated: type?, ?, ? T-cell mediated: type ?

Summary : 

Summary Therapy for type?hypersensitivity: Allergen avoidance Hyposensitivity Drug treatment: antihistamines, adrenaline

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Slide 41: 

Clustering of IgE receptors

Slide 42: 

Patholo-gical changes in asthma

Slide 43: 

An atopic eczema reaction

Slide 44: 

ADCC mediated by NK

Slide 45: 

The ABO system

Slide 46: 

Histology of acute inflammatory reaction in type ? hypersensitivity

Slide 47: 

IgE mediated mast cell activation and degranulation

Slide 48: 

Skin reaction of atopic allergy (Skin prick tests)

Slide 49: 

Deposition of immune complex in the kidney glomerulus

Slide 50: 

Vasculitic skin rashes due to immune complex deposition

Slide 51: 

Granuloma in tuberculosis infection

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