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Hypersensitivity Reactions Basics

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Hypersensitivity Reactions Basics

Hypersensitivity Reactions Basics


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  • 1. Hypersensitivity Reactions basics Dr.T.V.Rao MD Dr.T.V.Rao MD 1
  • 2. Hypersentivity Reactions Allergies Greek = altered reactivity 1906 – von Pirquet coined term: hypersensitivityHypersensitivity reactions – ‘over reaction’ of the immune system to harmless environmental antigens Dr.T.V.Rao MD 2
  • 3. Definition• Definition : Hypersensitivity refers to the injurious consequences in the sensitized host ,Following contact with specific Antigen Dr.T.V.Rao MD 3
  • 4. 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. Dr.T.V.Rao MD 4
  • 5. Hypersensitivity Immunity protects against Infections, Toxins. Many other functions.But Immunity can be Injurious,When exaggerated causes Tissue Damage, Disease and Death Dr.T.V.Rao MD 5
  • 6. Immune response is altered• In hypersensitivity Antigen is not Important But what happens as a result of Immune reaction• Allergy a Synonym for Hypersensitivity. Dr.T.V.Rao MD 6
  • 7. 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. Dr.T.V.Rao MD 7
  • 8. 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. Dr.T.V.Rao MD 8
  • 9. Hypersensitivity reactionsType Mechanism Antigen Onset IgE-Ag triggersI Allergen minutes Mast cell mediators IgG or IgM binds to Cell surfaceII Few cell surface; ADCC molecule hours or complement Immune complexes, Soluble or FewIII inflammation particulate hours Cytokines (T cells, Chemicals, 1-3IV Macrophages, CTL) intracellular days Dr.T.V.Rao MD 9
  • 10. Classification of Hypersensitivity• Immediate and Delayed. Immediate type Also called as Immediate HypersensitivityPopularly called as B cell MediatedHypersensitivity Dr.T.V.Rao MD 10
  • 11. Examples of Immediate Hypersensitivity• Anaphylaxis• Atopy,• Antibody mediated cell damage.• Arthus Phenomenon• Serum sickness Dr.T.V.Rao MD 11
  • 12. 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 Dr.T.V.Rao MD 12
  • 13. 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 1st pregnancy.• . Dr.T.V.Rao MD 13
  • 14. 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. Dr.T.V.Rao MD 14
  • 15. 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. Dr.T.V.Rao MD 15
  • 16. Delayed Hypersensitivity T Cell Mediated• Tuberculin type.• Contact dermatitis. Dr.T.V.Rao MD 16
  • 17. Type I Hypersensitivity Dr.T.V.Rao MD 17
  • 18. Examples of Immediate Hypersensitivity• Anaphylaxis• Atopy,• Antibody mediated cell damage.• Arthus Phenomenon• Serum sickness Dr.T.V.Rao MD 18
  • 19. Type I hypersensitivity• Anaphylaxis = Ana means without Phylaxis protection ( Rich )Sensitizing dose more effective when given parentallyAntigen can hapten also may take 2-3 weeks to produce sufficient IgE Shocking dose is effective if given IVThe nature of antigen should correspond to antibodies Dr.T.V.Rao MD 19
  • 20. 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) Dr.T.V.Rao MD 20
  • 21. 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 Dr.T.V.Rao MD 21
  • 22. 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 Dr.T.V.Rao MD 22
  • 23. 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 Dr.T.V.Rao MD 23
  • 24. 2nd dose produces Anaphylaxis • The 2nd produced anaphylactic shock • Manifested with Restlessness Chewing and rubbing nose Wheeze Developed convulsions Animal died Dr.T.V.Rao MD 24
  • 25. Same is experienced in Humans• With bee sting• Penicillin administration• Happens in sensitized individualsDr.T.V.Rao MD 25
  • 26. 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. Dr.T.V.Rao MD 26
  • 27. Nature of IgE• Present in low fractions compared with other Immunoglobulins• IgE is heat sensitive inactivated at 560c in 2 – 4 hours heat causes damage to Fc particle• IgA deficiency produces excessive IgE Dr.T.V.Rao MD 27
  • 28. Dr.T.V.Rao MD 28
  • 29. The biological mediator on effect stage1. Histamine: Dilate blood vessel Increase vascular permeability2. Leukotrienes: Bronchial smooth muscles contract Asthmas3. Prostaglandin: High concentration of PGE Inhibit the secretion of histamine low concentration of PGE promote the release of histamine4. Platelet activating factor (PAF) : Agglutinate and activate platelets to release histamine5. Eosinophil chemotactic factor(ECF-A):6. Bradykynin : Vasodilator function Dr.T.V.Rao MD 29
  • 30. 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. • Leukotrienes: Bronchial spasms.– Anaphylactic shock: Massive drop Dr.T.V.Rao MD 30
  • 31. 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 4. Skin allergy: Dr.T.V.Rao MD 31
  • 32. Atopy• When the antigen and antibody IgE react produce certain pharmacologically active substances Can cause Conjunctivitis, Rhinitis G E involvement Dermal involvement Urticaria Dr.T.V.Rao MD 32
  • 33. Dr.T.V.Rao MD 33
  • 34. p. 374Dr.T.V.Rao MD 34
  • 35. 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 Dr.T.V.Rao MD 35
  • 36. Effects of type I reactionsSystemic anaphylaxis Respiration becomes difficult Blood pressure drops Smooth muscles of bladder and GI tract contract BronchoconstrictionCountered by epinephrine relaxes smooth muscles decreases vascular permeability improves cardiac output Dr.T.V.Rao MD 36
  • 37. 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. Dr.T.V.Rao MD 37
  • 38. Histamine release occurs within minutes Binds to receptors on target cells smooth muscles contract eosinophils attracted mucus secretion platelet activation blood vessel dilationBlocked by various compounds: antihistamines,Epinephrine, corticosteroids Dr.T.V.Rao MD 38
  • 39. Secondary mediators of Anaphylaxis• Prostaglandins Leukotrienes• Thromboxanes,Lead to manifestation with1Transient constriction of Bronchioles2 Dilatation of capillaries,3 Platelet activation factor, Dr.T.V.Rao MD 39
  • 40. Serotonin• Produces on Decarboxylation of Tryptophan• Found in Intestines, Mucosa, Brain tissue, Platelets• Causes smooth muscle contraction• Increases capillary permeability• Vasoconstriction• Human ? Dr.T.V.Rao MD 40
  • 41. Other factors• Heparin Not in human• Enzymatic mediators proteases and hydrolases Dr.T.V.Rao MD 41
  • 42. Effects of Histamine Dr.T.V.Rao MD 42
  • 43. Many of us suffer Dr.T.V.Rao MD 43
  • 44. Secondary factors in anaphylaxis• Prostaglandins and Leukotrienes releases from disrupted cell membranes• Mast cells and other leukotrienes• Slow reacting substances• Prostaglandins affects secretion by mucosal glands• Platelet activating factor – aggregates platelets ad release vasoactive amines Dr.T.V.Rao MD 44
  • 45. 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
  • 46. Clinical effects• Causes smooth muscle contraction.• Increased vascular permeability• Many organs Target organ – shock organ• Causes Edema Fall of BP, Coagulation of Blood, Leucopenia, thrombocytopeniaGuinea pigs most susceptibleHumans IntermediateBee stings, Penicillin,Causes the constriction of smooth muscles( Bronchioles ) Dr.T.V.Rao MD 46
  • 47. 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 Dr.T.V.Rao MD 47
  • 48. 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
  • 49. Skin testsSkin test via intradermal injection ofallergens: if anindividual is allergicto the substanceinjected, local mastcells de granulateproducing a “wheeland flare” responsewithin minutes Dr.T.V.Rao MD 49
  • 50. Secondary Mediators of Anaphylaxis• Slow reacting substances• Prostaglandins,• Platelet activating factors Cytokines• IL3, IL4, IL5 Dr.T.V.Rao MD 50
  • 51. 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 Dr.T.V.Rao MD 51
  • 52. 5. Therapy of type I hypersensitivity 1. Allergen avoidance : Atopy patch test 2. Desensitivity therapy / Hyposensitization : 1) Allogenic serum desensitivity therapy: Repeated injection small amounts of allergen, Temporality 2) Specific allergen desensitivity therapy 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 : Dr.T.V.Rao MD 52
  • 53. Hypersensitivity type II Reactions Dr.T.V.Rao MD 53
  • 54. 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 Immunoglobulins or antibodies, usually long-lasting immunoglobulin G (IgG) antibodies. Dr.T.V.Rao MD 54
  • 55. 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. Dr.T.V.Rao MD 55
  • 56. 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 anemias 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 Dr.T.V.Rao MD 56
  • 57. Type II Hypersensitivity• LATS Antibodies stimulate determinants on Thyroid – Leads to excessive secretion of Thyroid hormones Dr.T.V.Rao MD 57
  • 58. 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. Dr.T.V.Rao MD 58
  • 59. 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 Dr.T.V.Rao MD 59
  • 60. Type II Hypersensitivity (Contd)• Anti erythrocyte antibodies• Autoimmune Anemias Hemolytic anemias.• Antigen + Antibody =Cell damage• Even Hap tens act in the place of Antigen• Disrupts the normal function• Graves disease , Myasthenia gravis. Dr.T.V.Rao MD 60
  • 61. Opsonization During Type-II Hypersensitivity, Step-1The Fab of IgG reacts with epitopes on the host cell membrane. PhagocytesMD Dr.T.V.Rao bind to the Fc 61 portion
  • 62. Opsonization During Type-II Hypersensitivity, Step-2Phagocytes binding to the Fc portion of the IgG and discharge their lysosomes causing cell Dr.T.V.Rao MD 62
  • 63. 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.• . Dr.T.V.Rao MD 63
  • 64. Good pastures syndrome• Good pastures syndrome: Generally manifested as a glomerulonephritis, IgG antibodies that react against glomerular basement membrane surfaces can lead to kidney destruction Dr.T.V.Rao MD 64
  • 65. 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 Dr.T.V.Rao MD 65
  • 66. Type III Hypersensitivity Reactions Dr.T.V.Rao MD 66
  • 67. Introduction• Immune complexes(Ag and Ab) deposit in tissues such as blood vessels and glomeruli.• activate complement, and cause tissue injury or dysfunctional responses. Dr.T.V.Rao MD 67
  • 68. 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 Dr.T.V.Rao MD 68
  • 69. 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. Dr.T.V.Rao MD 69
  • 70. 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 Dr.T.V.Rao MD 70
  • 71. 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 Dr.T.V.Rao MD 71
  • 72. Type III Hypersensitivity mechanism Neutrophil C3a & C5a C3C3b & C5b C4 C2 C1C5-C9 Dr.T.V.Rao MD 72
  • 73. 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 Dr.T.V.Rao MD 73 sulphonamides
  • 74. Mechanism of damage in type-III hypersensitivity Dr.T.V.Rao MD 74
  • 75. Deposition of immune complexes in blood vessel walls Dr.T.V.Rao MD 75
  • 76. Disorders of the Immune System: Immune Complex Disease Glomerular basement membrane of kidney Large complex Endothelial cell Small complex Dr.T.V.Rao MD 76
  • 77. Type III Hypersensitivity (Cont )• Serum Sickness –Systematic form of Type IIIDiphtheria Antiserum produces antibodiesProduces Fever, Lymphadenopathy Splenomegaly Arthritis Glomerulonephritis Endocarditis and VasculitisMechanism – Foreign serum and antibodies Deposit in Endothelial Lining on Blood vessels.Many times self limited. Dr.T.V.Rao MD 77
  • 78. Dr.T.V.Rao MD 78
  • 79. 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. Dr.T.V.Rao MD 79
  • 80. 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. Dr.T.V.Rao MD 80
  • 81. Type IV Hypersensitivity Dr.T.V.Rao MD 81
  • 82. 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 Dr.T.V.Rao MD 82
  • 83. 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 Dr.T.V.Rao MD 83
  • 84. 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 Dr.T.V.Rao MD 84
  • 85. Dr.T.V.Rao MD 85
  • 86. 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. Dr.T.V.Rao MD 86
  • 87. 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). Dr.T.V.Rao MD 87
  • 88. 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 Dr.T.V.Rao MD 88
  • 89. Mechanisms of damage in delayed hypersensitivity Dr.T.V.Rao MD 89
  • 90. 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 Dr.T.V.Rao MD 90
  • 91. Tuberculin Type ( IV )• Tuberculin reaction.• Tuberculin Injection• Sensitized to Tuberculin protein.• Indurations develop at the site < 48 hours.• Unsensitized No responseBacteria, Fungi, Viruses, Parasites Dr.T.V.Rao MD 91
  • 92. Tuberculin Test Dr.T.V.Rao MD 92
  • 93. Measurement of Induration Dr.T.V.Rao MD 93
  • 94. Immune Complex Mediated Hypersensitivity Dr.T.V.Rao MD 94
  • 95. 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 Dr.T.V.Rao MD 95
  • 96. Dr.T.V.Rao MD 96
  • 97. 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 Dr.T.V.Rao MD 97
  • 98. DTH as a result of a contact-sensitizing agent* Contact Dermatitis Can be caused by poison ivy and mango sap*a contact-sensitizing agent is usually a small molecule thatpenetrates the skin then binds to self-proteins, making theprotein “look” foreign Dr.T.V.Rao MD 98
  • 99. 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). Dr.T.V.Rao MD 99
  • 100. Contact Dermatitis ( IV )• Delayed hypersensitivity – Skin contact.• Cell Mediated response.• Nickel, Chromium, Dyes , Penicillins• Antigens absorbed,• Langerhams cells capture – Migrate to draining lymph nodes,• Present the processed Antigens with MHC molecules to Immune cells. Dr.T.V.Rao MD 100
  • 101. • 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