hypersensitivity reactions basics

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Hypersensitivity Reactions Basics


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Hello doctor, I am an MPH graduate. Can I have the leptospirosis an update ppt for academic purpose. my id is doctorbk@gmail.com. BK

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Hypersensitivity Reactions basics:

Hypersensitivity Reactions basics Dr.T.V.Rao MD 1 Dr.T.V.Rao MD

Hypersentivity Reactions:

Hypersentivity Reactions Allergies Greek = altered reactivity 1906 – von Pirquet coined term: hypersensitivity Hypersensitivity reactions – ‘over reaction’ of the immune system to harmless environmental antigens 2 Dr.T.V.Rao MD


Definition Definition : Hypersensitivity refers to the injurious consequences in the sensitized host ,Following contact with specific Antigen 3 Dr.T.V.Rao MD

How we classify Hypersensitivity:

How we classify Hypersensitivity Hypersensitivity refers to undesirable (damaging, discomfort-producing and sometimes fatal) reactions produced by the normal immune system. Hypersensitivity reactions require a pre-sensitized (immune) state of the host. Hypersensitivity reactions can be divided into four types: type I, type II, type III and type IV, based on the mechanisms involved and time taken for the reaction. 4 Dr.T.V.Rao MD


Hypersensitivity Immunity protects against Infections, Toxins. Many other functions. But Immunity can be Injurious, When exaggerated causes Tissue Damage, Disease and Death 5 Dr.T.V.Rao MD

Immune response is altered:

Immune response is altered In hypersensitivity Antigen is not Important But what happens as a result of Immune reaction Allergy a Synonym for Hyp ersensitivity. 6 Dr.T.V.Rao MD

What happens in Hypersensitivity:

What happens in Hypersensitivity Initial contact sensitizes the Immune system. The antigen acts as priming dose Causes the priming of B/T Lymphocytes , Subsequent dose a shocking dose. 7 Dr.T.V.Rao MD

Classification of Hypersensitivity Coombs and Gell:

Classification of Hypersensitivity Coombs and Gell Classified into 4 types on Mechanism and Pathogenicity Type I Generalized – Anaphylactic shock. Localized - Hay fever, Asthma Type II Cytotoxic ( Antigen + Antibody ) Type III Immune complex Type IV Cell Mediated. 8 Dr.T.V.Rao MD

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Hypersensitivity reactions Type Mechanism Antigen Onset I IgE-Ag triggers Mast cell mediators Allergen minutes II IgG or IgM binds to cell surface; ADCC or complement Cell surface molecule Few hours III Immune complexes, inflammation Soluble or particulate Few hours IV Cytokines (T cells, Macrophages, CTL) Chemicals, intracellular 1-3 days 9 Dr.T.V.Rao MD

Classification of Hypersensitivity:

Classification of Hypersensitivity Immediate and Delayed. Immediate type Also called as Immediate Hypersensitivity Popularly called as B cell Mediated Hypersensitivity 10 Dr.T.V.Rao MD

Examples of Immediate Hypersensitivity:

Examples of Immediate Hypersensitivity Anaphylaxis Atopy, Antibody mediated cell damage. Arthus Phenomenon Serum sickness 11 Dr.T.V.Rao MD


12 Hypersensitivity-1 Inappropriate immune responses Type I are immediate type, in which antigen binds to IgE on mast cells, histamine released. Histamine: smooth muscle contraction, vasodilatation. Results in asthma, diarrhea, shock depending on where antigen enters body. Ex. Bee sting 12 Dr.T.V.Rao MD

Type II Hypersentivity:

Type II Hypersentivity Type II are cytotoxic reactions like the Rh factor problem and bad blood transfusions. Rh is one of many blood groups, like ABO An Rh+ fetus in an Rh- mother means she gets immunized by baby’s blood cells, makes Antibodies. Second pregnancy, fetal RBCs are attacked. Solution: give Rho-gam during 1 st pregnancy. . 13 Dr.T.V.Rao MD

Type III and IV:

Type III and IV Type III are immune complex disorders, where too many agn-aby clumps cause inflammation Type IV are delayed type, T cell produces various cytokines which affect macrophages. 14 Dr.T.V.Rao MD

Type IV:

15 Type IV Type IV are delayed type, T cell produces various cytokines which affect macrophages. The bar fight scenario: come, stay, get angry. Angry macrophages cause much tissue damage. Ex. Poison ivy; urushiol-coated cells killed. 15 Dr.T.V.Rao MD

Delayed Hypersensitivity T Cell Mediated :

Delayed Hypersensitivity T Cell Mediated Tuberculin type. Conta ct derma titis. 16 Dr.T.V.Rao MD

Type I Hypersensitivity:

Type I Hypersensitivity Dr.T.V.Rao MD 17

Examples of Immediate Hypersensitivity:

Examples of Immediate Hypersensitivity Anaphylaxis Atopy, Antibody mediated cell damage. Arthus Phenomenon Serum sickness 18 Dr.T.V.Rao MD

Type I hypersensitivity:

Type I hypersensitivity Anaphylaxis = Ana means without Phylaxis protection ( Rich ) Sensitizing dose more effective when given parentally Antigen can hapten also may take 2-3 weeks to produce sufficient IgE Shocking dose is effective if given IV The nature of antigen should correspond to antibodies 19 Dr.T.V.Rao MD

Type I:

Type I Anaphylactic Ig E ( Reagin ) Antibodies are fixed on Tissue cells Eg Mast cells and Basophils Antigen + Antibody combination causes release of Pharmacologically active substances Occurs in Acute and Chronic or recurrent form (Non Fatal and localized Atopy) 20 Dr.T.V.Rao MD

Anaphylaxis :

Anaphylaxis Classical Immediate Hypersensitivity Experiments in dogs with Sea anemones Guinea pigs By any route with Antigens and Haptens 2-3 weeks later with sensitizing or shocking dose I V 21 Dr.T.V.Rao MD

The type I – anaphylaxis involves:

The type I – anaphylaxis involves The target organs are several vital organs and tissues, On the target tissue, causes oedema,decreased coagabulity of Blood Leads to fall of Blood pressure Leucopenia and thrombocytopenia Guinea pigs are highly sensitive Human are intermediate in reactivity 22 Dr.T.V.Rao MD

Experiment in Guinea pig:

Experiment in Guinea pig A guinea pig is injected with small dose of antigen eg Egg albumin no reaction observed. The same animal injected with egg albumin after 2 weeks by IV route 23 Dr.T.V.Rao MD

2nd dose produces Anaphylaxis:

2 nd dose produces Anaphylaxis The 2 nd produced anaphylactic shock Manifested with Restlessness Chewing and rubbing nose Wheeze Developed convulsions Animal died 24 Dr.T.V.Rao MD

Same is experienced in Humans:

Same is experienced in Huma ns With bee sting Penicillin administration Happens in sensitized individuals 25 Dr.T.V.Rao MD

Local reactions happen:

Local reactions happen Asthma Hay fever The reactions depend on the level of IgE The biologically active molecules are present in in the mast cells and Basophilic granules synthesize to active production after triggering with antigenic stimulations. 26 Dr.T.V.Rao MD

Nature of IgE:

Nature of IgE Present in low fractions compared with other Immunoglobulin's IgE is heat sensitive inactivated at 56 0 c in 2 – 4 hours heat causes damage to Fc particle IgA deficiency produces excessive IgE Dr.T.V.Rao MD 27

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The biological mediator on effect stage 1. Histamine: Dilate blood vessel Increase vascular permeability 2. Leukotriene's: Bronchial smooth muscles contract Asthmas 3. Prostaglandin: High concentration of PGE Inhibit the secretion of histamine low concentration of PGE promote the release of histamine 4. Platelet activating factor (PAF) : Agglutinate and activate platelets to release histamine 5 . Eosinophil chemotactic factor ( ECF-A): 6. Bradykynin : Vasodilator function 29 Dr.T.V.Rao MD

Important chemical and substances produced to cause reaction:

Important chemical and substances produced to cause reaction Histamine: Dilates and increases permeability of blood vessels (swelling and redness), increases mucus secretion (runny nose), smooth muscle contraction (bronchi). Prostaglandins: Contraction of smooth muscle of respiratory system and increased mucus secretion. Leukotriene's: Bronchial spasms. Anaphylactic shock: Massive drop 30 Dr.T.V.Rao MD

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4 . Skin allergy: 4 . Common disease of type I hypersensitivity 1 .  Systemic anaphylaxis: a very dangerous syndrome 1) Anaphylactic drug allergy : penicillin 2) Anaphylactic serum allergy : 2 . Respiratory allergic diseases : 1) Allergic asthma : acute response, chronic response 2) Allergic rhinitis 3 . Gastrointestinal allergic diseases : The lack of SIgA protein hydrolase Undigested protein Allergen 31 Dr.T.V.Rao MD


Atopy When the antigen and antibody IgE react produce certain pharmacologically active substances Can cause Conjunctivitis, Rhinitis G E involvement Dermal involvement Urticaria 32 Dr.T.V.Rao MD

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p. 374 34 Dr.T.V.Rao MD

Primary Mediators of Anaphylaxis:

Primary Mediators of Anaphylaxis Histamine an vasoactive in human Anaphylaxis Histidine on Decarboxylation to Histamine Stimulates the sensory nerves Causes burning and itching Causes vasodilatation and hyperemia Smooth muscle stimulation Affects the Intestines, Uterus, Especially bronchioles 35 Dr.T.V.Rao MD

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Effects of type I reactions Systemic anaphylaxis Respiration becomes difficult Blood pressure drops Smooth muscles of bladder and GI tract contract Bronchoconstriction Countered by epinephrine relaxes smooth muscles decreases vascular permeability improves cardiac output 36 Dr.T.V.Rao MD

Mechanism of Anaphylaxis :

Mechanism of Anaphylaxis Ig E cell fixed on Mast cells and Basophiles. Antigen + Antibody Bridges the gap Leads to deregulation Releases Biologically active substances from granules of the cells. 37 Dr.T.V.Rao MD

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Histamine release occurs within minutes Binds to receptors on target cells smooth muscles contract eosinophil's attracted mucus secretion platelet activation blood vessel dilation Blocked by various compounds: antihistamines, Epinephrine, corticosteroids 38 Dr.T.V.Rao MD

Secondary mediators of Anaphylaxis:

Secondary mediators of Anaphylaxis Prostaglandins Leukotriene's Thromboxane's, Lead to manifestation with 1Transient constriction of Bronchioles 2 Dilatation of capillaries, 3 Platelet activation factor, 39 Dr.T.V.Rao MD


Serotonin Produces on Decarboxylation of Tryptophan Found in Intestines, Mucosa, Brain tissue, Platelets Causes smooth muscle contraction Increases capillary permeability Vasoconstriction Human ? 40 Dr.T.V.Rao MD

Other factors:

Other factors Heparin Not in human Enzymatic mediators proteases and hydrolases Dr.T.V.Rao MD 41

Effects of Histamine:

Effects of Histamine 42 Dr.T.V.Rao MD

Many of us suffer :

Many of us suffer 43 Dr.T.V.Rao MD

Secondary factors in anaphylaxis:

Secondary factors in anaphylaxis Prostaglandins and Leukotriene's releases from disrupted cell membranes Mast cells and other leukotriene's Slow reacting substances Prostaglandins affects secretion by mucosal glands Platelet activating factor – aggregates platelets ad release vasoactive amines 44 Dr.T.V.Rao MD

Other Mediators:

Other Mediators By complement activation Bradykynin Anphylactoid reactions can be caused due to IV Peptone, Trypsin by IV routes Dr.T.V.Rao MD 45

Clinical effects:

Clinical effects Causes smooth muscle contraction. Increased vascular permeability Many organs Target organ – shock organ Causes Edema Fall of BP, Coagulation of Blood, Leucopenia, thrombocytopenia Guinea pigs most susceptible Humans Intermediate Bee stings, Penicillin, Causes the constriction of smooth muscles( Bronchioles ) 46 Dr.T.V.Rao MD

Clinical effects in Humans:

Clinical effects in Humans Itching of scalp, Tongue Flushing of skin, Bronchial spasm Hypotension Loss of consciousness and Death Previously with serum Now with Antibiotics. Adrenaline is life saving 0.5 ml 1:1000 dils 47 Dr.T.V.Rao MD

Clinical effects Cutaneous Anaphylaxis:

Clinical effects Cutaneous Anaphylaxis Intradermal Injection in sensitized host Wheal and flare reaction Useful in skin testing ( But dangerous ) Passive cutaneous anaphylaxis. Dr.T.V.Rao MD 48

Skin tests:

Skin tests Skin test via intra dermal injection of allergens: if an individual is allergic to the substance injected, local mast cells de granulate producing a “wheel and flare” response within minutes 49 Dr.T.V.Rao MD

Secondary Mediators of Anaphylaxis:

Secondary Mediators of Anaphylaxis Slow reacting substances Prostaglandins, Platelet activating factors Cytokines IL3, IL4, IL5 Dr.T.V.Rao MD 50


Atopy Agent Inhaled – Pollens /Dust Ingested – Egg , Milk Contact with skin – Conjunctiva Ig E is over produced Bottle fed infants Estimation of Ig E by RAST 51 Dr.T.V.Rao MD

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5. Therapy of type I hypersensitivity 1 .   Allergen avoidance : Atopy patch test 2.   Desensitivity therapy / Hyposensitization : 1) Allogenic serum desensitivity therapy: 2) Specific allergen desensitivity therapy Repeated injection small amounts of allergen, T emporality IgG+allergen Neutralizing antibody, Blocking antibody 3.   Drug therapy : 1 ) Stabilization of triggering cells sodium cromoglycate stabilize the membrane, inhibit mast cell degranulation 2 ) Mediator antagonism Chlor-Trimeton Antihistamine Acetylsalicylic acid Bradykinin antagonism 3) Improve the responsibility of target organs 4.   New immunotherapy : 52 Dr.T.V.Rao MD

Hypersensitivity type II Reactions:

Hypersensitivity type II Reactions 53 Dr.T.V.Rao MD

Type II Hypersensitivity:

Type II Hypersensitivity Type II hypersensitivity or cytotoxic hypersensitivity is caused by antibody-mediated reactions. When the immune system reacts to antigens it produces various Immunoglobulin's or antibodies, usually long-lasting immunoglobulin G (IgG) antibodies. 54 Dr.T.V.Rao MD

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Type II (Cytotoxic) Reactions Involve activation of complement by IgG or IgM binding to an antigenic cell. Antigenic cell is lysed. Transfusion reactions: ABO Blood group system: Type O is universal donor. Incompatible donor cells are lysed as they enter bloodstream. Rh Blood Group System: 85% of population is Rh positive. Those who are Rh negative can be sensitized to destroy Rh positive blood cells. Hemolytic disease of newborn: Fetal cells are destroyed by maternal anti-Rh antibodies that cross the placenta. 55 Dr.T.V.Rao MD

What Happens in type II:

What Happens in type II Ig G and Ig M combines with antigenic determinants on the cells. Leads to cytotoxic and catalytic effects Eg - Anti erythrocyte antibodies in autoimmune anemia's and hemolytic disease of the new born. Other free antigens or hapten may be absorbed on the cell surface Subsequent reactions will lead to cell damage Drugs too behave in the same way 56 Dr.T.V.Rao MD

Type II Hypersensitivity :

Type II Hypersensitivity LATS Antibodies stimulate determinants on Thyroid – Leads to excessive secretion of Thyroid hormones 57 Dr.T.V.Rao MD

Haptens too can produce type II Hypersensitivity:

Haptens too can produce type II Hypersensitivity . The antigens are normally endogenous, although exogenous chemicals ( haptens ) which can attach to cell membranes can also lead to type II hypersensitivity. 58 Dr.T.V.Rao MD

Type II Hypersensitivity:

Type II Hypersensitivity The binding of these antibodies to the surface of host cells then leads to: opsonization of the host cells whereby phagocytes stick to host cells by way of IgG, C3b, or C4b and discharge their lysosomes 59 Dr.T.V.Rao MD

Type II Hypersensitivity (Contd):

Type II Hypersensitivity (Contd) Anti erythrocyte antibodies Autoimmune Anemia's Hemolytic anemia's. Antigen + Antibody =Cell damage Even Hap tens act in the place of Antigen Disrupts the normal function Graves disease , Myasthenia gravis. 60 Dr.T.V.Rao MD

Opsonization During Type-II Hypersensitivity, Step-1 :

Opsonization During Type-II Hypersensitivity, Step-1 The Fab of IgG reacts with epitopes on the host cell membrane. Phagocytes bind to the Fc portion 61 Dr.T.V.Rao MD

Opsonization During Type-II Hypersensitivity, Step-2 :

Opsonization During Type-II Hypersensitivity, Step-2 Phagocytes binding to the Fc portion of the IgG and discharge their lysosomes causing cell lysis. 62 Dr.T.V.Rao MD

Examples of Type II Hypersensitivity. :

Examples of Type II Hypersensitivity. Pemphigus: IgG antibodies that react with the intracellular substance found between epidermal cells. Autoimmune haemolytic anaemia (AHA): This disease is generally inspired by a drug such as penicillin that becomes attached to the surface of red blood cells (RBC) and acts as hapten for the production of antibody which then binds the RBC surface leading to lysis of RBCs. . 63 Dr.T.V.Rao MD

Good pasture's syndrome:

Good pasture's syndrome Good pasture's syndrome: Generally manifested as a glomerulonephritis, IgG antibodies that react against glomerular basement membrane surfaces can lead to kidney destruction 64 Dr.T.V.Rao MD

Type II Hypersensitivity:

Type II Hypersensitivity Salmonella , and Mycobacterium can produce Hemolytic crisis Diagnostic tests include detection of circulating antibody against the tissues involved and the presence of antibody and complement in the lesion (biopsy) by immunofluorescence 65 Dr.T.V.Rao MD

Type III Hypersensitivity Reactions:

Type III Hypersensitivity Reactions 66 Dr.T.V.Rao MD


Introduction Immune complexes(Ag and Ab) deposit in tissues such as blood vessels and glomeruli. activate complement, and cause tissue injury or dysfunctional responses. 67 Dr.T.V.Rao MD

Arthus reaction:

Arthus reaction Injecting repeatedly sc Normal horse serum Later injections leads edema, indurations hemorrhagic necrosis manifest as localize from of generalized hypersensitivity Damage is caused due to Antigen and antibody complexes, leads to activation of complement Release of inflammatory molecules Vascular permeability, infiltration of neutrophils. Causes tissue necrosis Eg Inhalation of Actinomyctes from mouldy hay grain causes Farmer’s lung 68 Dr.T.V.Rao MD

Type III Hypersensitivity:

Type III Hypersensitivity Example of a Type III hypersensitivity is serum sickness , a condition that may develop when a patient is injected with a large amount of e.g. antitoxin that was produced in an animal. After about 10 days, anti-antitoxin antibodies react with the antitoxin forming immune complexes that deposit in tissues. 69 Dr.T.V.Rao MD

Type III hypersensitivity:

Type III hypersensitivity Type III hypersensitivity is also known as immune complex hypersensitivity. The reaction may be general ( e.g. , serum sickness) or may involve individual organs including skin ( e.g. , systemic lupus erythematous, Arthurs reaction), kidneys ( e.g. , lupus nephritis), lungs ( e.g. , Aspergillosis ), blood vessels ( e.g. , polyarteritis ), joints ( e.g. , rheumatoid arthritis) or other organs. This reaction may be the pathogenic mechanism of diseases caused by many microorganism 70 Dr.T.V.Rao MD

Type III Hypersensitivity:

Type III Hypersensitivity Antigen and Antibody complexes Accumulate around the small blood vessels cause damage to cell Arthus Reaction Occurs as a local manifestation Antigen + Antibody complexes Releases Inflammatory molecules, Infiltration with Neutrophils Reduces blood supply Other example – Inhaled antigens produce Farmers lung 71 Dr.T.V.Rao MD

Type III Hypersensitivity mechanism:

Y Y Y Y Neutrophil C1 C2 C4 C3b & C5b C5-C9 C3 C3a & C5a Type III Hypersensitivity mechanism 72 Dr.T.V.Rao MD

2- Serum Sickness :

2- Serum Sickness * A systemic immune complex phenomenon * Injection of large doses of foreign serum * Antigen is slowly cleared from circulation * Immune complexes are deposited in various sites fever urticaria * 10 days after injection Arthralgia lymphadenopathy splenomegaly glomerulonephritis antidiphtheritic serum e.g. treatment with penicillin sulphonamides 73 Dr.T.V.Rao MD

Mechanism of damage in type-III hypersensitivity:

Mechanism of damage in type-III hypersensitivity 74 Dr.T.V.Rao MD

Deposition of immune complexes in blood vessel walls:

Deposition of immune complexes in blood vessel walls 75 Dr.T.V.Rao MD

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Disorders of the Immune System: Immune Complex Disease Glomerular basement membrane of kidney Large complex Endothelial cell Small complex 76 Dr.T.V.Rao MD

Type III Hypersensitivity (Cont ):

Type III Hypersensitivity (Cont ) Serum Sickness – Systematic form of Type III Diphtheria Antiserum produces antibodies Produces Fever, Lymphadenopathy Splenomegaly Arthritis Glomerulonephritis Endocarditis and Vasculitis Mechanism – Foreign serum and antibodies Deposit in Endothelial Lining on Blood vessels. Many times self limited. 77 Dr.T.V.Rao MD

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Serum Sickness :

Serum Sickness May last for 7-10 days. Bacterial Viral and Parasitic infection produce serum sickness. Important Diseases Post Streptococcal Glomerulonephritis Hepatitis B Infections Auto immune conditions. Disseminate malignancies. 79 Dr.T.V.Rao MD

Diagnosis and Treatment:

Diagnosis and Treatment The presence of immune complexes in serum and depletion in the level of complement are also diagnostic. Polyethylene glycol-mediated turbidity (Nephelometry), binding of C1q and Raji cell test are utilized to detect immune complexes. Treatment includes anti-inflammatory agents. 80 Dr.T.V.Rao MD

Type IV Hypersensitivity:

Type IV Hypersensitivity 81 Dr.T.V.Rao MD

Type IV Hypersensitivity:

Type IV Hypersensitivity Type IV hypersensitivity is often called delayed type hypersensitivity as the reaction takes two to three days to develop. Unlike the other types, it is not antibody mediated but rather is a type of cell-mediated response 82 Dr.T.V.Rao MD

Type IV Reaction Delayed Hypersensitivity:

Type IV Reaction Delayed Hypersensitivity Also called as Cell Mediated Immunity, Stimulates – Sensitizes CD4/CD8. Secretion of Lymhokines Fluid/Phagocytes accumulate. Not Induced by antibodies T Cell Th1 Th2 Tc Take active part 83 Dr.T.V.Rao MD

Delayed hypersensitivity. :

Delayed hypersensitivity . The reaction elicited by antigen occurs relatively slowly (hence the name "delayed hypersensitivity"). The hypersensitivity is mediated via T-cells and macrophages. The hypersensitivity illustrates both antigen-specific (T-cell) and antigen non-specific (macrophage) characteristics 84 Dr.T.V.Rao MD

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Type IV hypersensitivity is T cell mediated:

Type IV hypersensitivity is T cell mediated The type IV hypersensitivity differs from the other three types of reactions in that it is not caused by antibodies, but by immunocompetent cells (lymphocytes). These lymphocytes are immunologically specific with receptors for the antigens, which can be different tissues (tissue antigens) or small molecular substances which, when fixed to the cell membrane, can function as antigens. 86 Dr.T.V.Rao MD

Type IV Reactions:

Type IV Reactions Type IV reactions, which are also called delayed hypersensitivity reactions, as a rule occur 12 - 48 hours after exposure to the antigen. Type IV reactions lead to inflammatory tissue damage and infiltration of cells, which are principally mononuclear (lymphocytes and macrophages). 87 Dr.T.V.Rao MD

Type IV reactions:

Type IV reactions The inflammatory reaction leads to irreversible damage with deterioration of the tissue. The classical examples of type IV hypersensitivity are the positive tuberculin reaction , contact dermatitis (e.g. caused by nickel or chrome) and rejection of tissues transplanted from other individual 88 Dr.T.V.Rao MD

Mechanisms of damage in delayed hypersensitivity:

Mechanisms of damage in delayed hypersensitivity 89 Dr.T.V.Rao MD

Several diseases based on Delayed Hypersensitivity:

Several diseases based on Delayed Hypersensitivity Type IV hypersensitivity is involved in the pathogenesis of many autoimmune and infectious diseases (tuberculosis, leprosy, blastomycosis, Histoplasmosis, toxoplasmosis, leishmaniasis, etc. ) granulomas due to infections and foreign bodies 90 Dr.T.V.Rao MD

Tuberculin Type ( IV ):

Tuberculin Type ( IV ) Tuberculin reaction. Tuberculin Injection Sensitized to Tuberculin protein. Indurations develop at the site < 48 hours. Unsensitized No response Bacteria, Fungi, Viruses, Parasites 91 Dr.T.V.Rao MD

Tuberculin Test:

Tuberculin Test 92 Dr.T.V.Rao MD

Measurement of Induration :

Measurement of Induration 93 Dr.T.V.Rao MD

Immune Complex Mediated Hypersensitivity:

Immune Complex Mediated Hypersensitivity 94 Dr.T.V.Rao MD

Other agents stimulating Type IV Hypersensitivity:

Other agents stimulating Type IV Hypersensitivity Topical application of Penicillin in creams Lange ham cells in epidermis absorb the drug or chemical T Cells are stimulated Lymph nodes acts as store houses Repeated applications leads to Eczema like conditions 95 Dr.T.V.Rao MD

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3. Common disease of type IV hypersensitivity 1) Infectious delayed type hypersensitivity OT( Old Tuberculin ) test 2) Contact dermatitis : Paint, drug red rash, papula, water blister, dermatitis 3) Acute rejection of allogenic transplantation and immune response in local tumor mass Same disease (SLE), multiple immune injury ,hypersensitivity involved Same drug (penicillin), several types of hypersensitivity 97 Dr.T.V.Rao MD

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*a contact-sensitizing agent is usually a small molecule that penetrates the skin then binds to self-proteins, making the protein “look” foreign Can be caused by poison ivy and mango sap Contact Dermatitis DTH as a result of a contact-sensitizing agent* 98 Dr.T.V.Rao MD

Contact dermatitis:

Contact dermatitis Contact dermatitis or Irritant dermatitis is a term for a skin reaction resulting from exposure to allergens (allergic contact dermatitis) or irritants (irritant contact dermatitis). 99 Dr.T.V.Rao MD

Contact Dermatitis ( IV ):

Contact Dermatitis ( IV ) Delayed hypersensitivity – Skin contact. Cell Mediated response. Nickel, Chromium, Dyes , Penicillin's Antigens absorbed, Langerhams cells capture – Migrate to draining lymph nodes, Present the processed Antigens with MHC molecules to Immune cells. 100 Dr.T.V.Rao MD

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Created by Dr.T.V.Rao MD for Undergraduate Medical and Paramedical students in the Developing world Email doctortvrao@gmail.com Dr.T.V.Rao MD 101

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