Hypersensitivity

Mark Christian D. Duatin, RMT your name

HYPERSENSITIVITY 
An abnormal response to antigens An exaggerated response to an innocuous antigen that results in gross tissue changes that are deleterious to the host.

Hypersensitivity

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Gell and Coombs Classification
‡ Type I (Anaphylactic) Reactions ‡ Type II (Cytotoxic) Reactions ‡ Type III (Immune Complex) Reactions ‡ Type IV (Cell-Mediated) Reactions

Hypersensitivity

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Type I (Anaphylactic) Reactions
± Occur within minutes of exposure to antigen ± Atopic Antigens/Allergens combine with IgE antibodies ± IgE binds to mast cells and basophils, causing them to undergo degranulation and release several mediators:
Hypersensitivity
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Mast Cells and the Allergic Response Hypersensitivity your name .

5. 9 and 13 overproduction of mucusname your Hypersensitivity .13 IL-4 and IL-13 class switching IL-5 and IL-9 development of eosinophils IL-4 and IL-9 development of mast cells Il-4.9.Th1 produces interferon-gamma Macrophages produce interluekin-12 and interleukin-18 *** Suppress production of IgE type antibodies Th2 produces interleukin-4.

Sensitization phase » IgE produced in response to antigenic stimulus & binds to receptors on mast cells and basophils 2. Effector phase » Complex response occurs as a result of histamine & other pharmacologically active agents released by mast cells & basophils Hypersensitivity your name . Activation phase » Re-exposure to antigen triggers mast cells and basophils to respond by release of their granules 3.PHASES 1.

erythema and wheal and flare formation Chemotactic factors  eosinophilic chemotactic factor (ECF)  IL-3. vasodilation (H2 receptors)  Mucus secretion . 4 & 5 Heparin .Preformed Mediators Histamine  Smooth muscle: contraction (H1 receptors)  Endothelial cells: vascular permeability.inhibits coagulation Hypersensitivity your name .gut & respiratory epithelial  Skin.

vasodilation Hypersensitivity your name .Newly Synthesized Mediators  Leukotrienes .smooth muscle contraction (prolonged) Thromboxanes & prostaglandins ± bronchoconstriction.

Manifestations Anaphylaxis Allergic asthma Allergic rhinitis Allergic urticaria Atopic dermatitis Hypersensitivity your name .

Allergic asthma: (extrinsic asthma) characterized BRONCHOSPASM. It may be caused by injection of anti tetanic horse serum. there is a complete vasomotor collapse and bronchoconstriction. eosinophilia in blood and sputum Hypersensitivity your name .Anaphylaxis: BRONCHOCONSTRICTION symptoms is the inability to breathe. penicillin or bee sting.

Eosinophilia may be present in nasal secretion caused by pollen. Allergic urticaria: (hives) characterized WHEALS (dermal edema). SNEZING and others. ERYTHEMA (reddening). Angioedema (severe local swelling) around the face and sometimes respiratory obstruction due to edema in the larynx and pharynx Hypersensitivity your name .Allergic arthritis: (hay fever) characterized WATERY NASAL DISCHARGE.

usually seen in infants or young children Hypersensitivity your name .Atopic dermatitis: (eczema) characterized PRURITIS (itching).

radioallergosorbent test Hypersensitivity your name .Detection of Allergies ‡ Skin Test ‡ Blood Test ± Elevated IgE (ELISA) ± RIST Test .radioimmunosorbant test ± RAST Test .

Epinephrine .relaxes smooth muscle & decreases mast cell degranulation » reverses effects of anaphylaxis Immunologic your name Hypersensitivity ‡ Hyposensitization Treatments .Environmental Avoid exposure to ³it´ Pharmacologic 1. common treatment for asthmatics 5. Theophylline -prolongs cAMP production » blocks degranulation.compete for histamine for receptor sites » Prevents symptoms 2.stabilizes membranes » prevents Ca+2 influx.block synthesis of arachidonic acid & histamine levels » Prevent early & late phase reaction 4. Antihistamines . Corticosteroids . prevents mast cell degranulation if taken BEFORE exposure 3. Cromolyn sodium .

Hypersensitivity your name .Type II (Cytotoxic) Reactions ‡ Reactants responsible are IgM and IgG ‡ They are triggered by antigens FOUND ON CELL SURFACES ‡ Antibody coats cellular surfaces and promotes phagocytosis by both opsonization and activation of the complement cascade.

‡ CLINICAL MANIFESTATIONS : ±transfusion reactions ±HDN ±AIHA ±DIHA Hypersensitivity your name .

Type II Reactions involving Tissue Antigen ‡ Goodpasteur¶s syndrome ‡ Grave¶s disease Hypersensitivity your name .

Hypersensitivity your name . and cause inflammatory damage. ± Antibody-Antigen immune complexes are deposited in organs. activate complement.Type III (Immune Complex) Reactions ± Involve reactions against soluble antigens circulating in serum.

Immune Complex Mediated Hypersensitivity Hypersensitivity your name .

‡ Arthus Reaction ‡ Serum Sickness ‡ Autoimmune Diseases ± SLE ± RA Hypersensitivity your name .

produce edema and enhance inflammation Hypersensitivity your name . including IL-2.Type IV : Delayed Hypersensitivity Reaction ‡ Sensitized T cells play the major role in its manifestation. ‡ T helper cells are activated and release cytokines. IFN-gamma and TNF-beta that recruit macrophages and neutrophils.

dyes.Contact Dermatitis ‡ Reaction usually due to lowmolecular weight compound that touches the skin. fabric finishes. medications Hypersensitivity your name . cosmetics. rubber. poison oak ‡ Other compounds includes nickel. ‡ Most common causes include poison ivy.

swelling.Contact Dermatitis *** The Langerhans cell functions as the APC The langerhans cells may migrate to the regional lymph nodes and generate sensitized cells there After Repeat exposure . a skin eruption characterized by erythema. and formation of papules appears from 6 hours to several days after exposure Hypersensitivity your name .

type Hypersensitivity ‡ Soluble antigens from Mycobacterium tuberculosis induce a reaction in people ho have or have had tuberculosis ‡ Previously sensitized individuals develop an area of erythema and induration at the site of injection ‡ Reaction peaks by 72 hours after exposure Hypersensitivity your name .Tuberculin.

END Hypersensitivity your name .

Cytokines ‡ Chemical messengers that influence the activities of other cells *** Autocrine *** Paracrine *** Endocrine Cytokines your name .

Features of Cytokines *** Pleiotrophy *** Redundancy Cytokines act in networks Cytokines may also produce effects that terminate their activities Many cytokines act as growth factors for hematopoietic cells Cytokines your name .

IFN. a. Interferons *** originally named because they interfere with viral replication in an infected cell.Cytokines in Innate Immune Response 1. IFN.>> produced by fibroblasts Cytokines your name .>> produced by mononuclear phagocytes b.

IFN ‡ Produced primarily during the initial innate response to viral infection Functions: Increase the ability of NK cells to kill virally infected cells Enhance expression of class I MHC Cytokines Hypersensitivity your name .Type 1.

Cytokines in Innate Immune Response 2. Tissue Necrosis Factor (TNF) *** Major mediator of the innate immune response against gram-negative bacteria Cytokines your name .

Interleukins Coined when it was thought that cytokines primarily served as a means of communication between leukocytes Cytokines your name .Cytokines in Innate Immune Response 3.

Interleukins IL-1 Produced by macrophages and monocytes Actions include inducing IL-2 and IL-2 receptors (CD25) in T cells. and enhancement of cytotoxicity of NK cells Acts as a chemotactic agent Cytokines your name . Proliferation and differentiation of B cells.

Interleukins IL-6 Primary mediator of the acute phase response *** signals for enhanced fibrinogen synthesis by the liver Growth factor for activated B lymphocytes and plasma cells Cytokines your name .

Inhibits functions of mononuclear phagocytes for T cell activation Cytokines your name .Interleukins IL-10 Primarily inhibitory effects on the immune system a. Inhibits production of proinflammatory cytokines b.

15 Release occurs in response to viral infection.Interleukins IL. or other products of pathogens that are recognized by the innate immune system Cytokines your name . LPS.

Cytokines in Innate Immune Response Chemokines ‡ Chemotactic cytokines that enhances motility and promotes the migration of specific classes of leukocytes towards the source of the chemokine Cytokines your name .

Cytokines in specific Immune Response ‡ The cytokines that promote and regulate innate IR are largely secreted by mononuclear phagocytes. the cytokines that regulate acquired IR are largely secreted by T cdells. especially T helper cells Cytokines your name . In contrast.

T cell proliferation and differentiation Eosinophil production and activation IL-4 Th cells and Mast cells IL-5 T cell IFN- T cells.Cytokines in specific Immune Response Name Primary Source Actions IL-2 T cells Proliferation and Activation of T. enhanced MHC on all cell types your name . NK cells Mononuclear phagocyte activation. B and NK cells Can promote apoptosis Isotype switching to IgE.

*** Primary mediators are CSF Cytokines your name .Hematopoietic Factors A numbe rof cytokines produced during innate and acquired immune response stimulate the proliferation and differentiation of bone marrow progenitor cells.

Hematopoietic Factors C-kit ligand/ stem cell factor Growth factor that affects the groth of the most primitive precursor cells in the bone marrow Has a role in maintaining the viability of T cells in the thymus and mast cells in mucosal sites Cytokines your name .

Hematopoietic Factors IL-3/ Multilineage CSF Produced by Th cells Stimulates the proliferation of immature marrow cells that are not yet committed to a specific lineage Cytokines your name .

END _oyo^ your name .

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