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HYPERSENSITIVITY
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                  Hypersensitivity overview
                  Classification of hypersensitivity
                  Type I Hypersensitivity
                      Anaphylaxis
                      Atopy
                  Type II Hypersensitivity
                      Blood transfusion reactions
                      Hemolytic disease of newborn
                      Drug induced hemolysis
                  Type III Hypersensitivity
                      Localized
                      Generalized
                  Type IV Hypersensitivity
                      Tuberculin reaction
                      Contact dermatitis
Hypersensitivity
• Hypersensitivity is the term used when an
  immune response results in exaggerated or
  inappropriate reaction harmful to the host.
Hypersensitivity
                    Antigen             Immunity

• Hypersensitivity is the term used when an
                              Antigen     Antigen
  immune response results in exaggerated killed
           Host                            or
  inappropriate reaction harmful to the host.
  Antigen




                                    ?
                                          Hypersensitivity
Common terms
• Allergen        Antigen ( bland substance
  like serum protein or pollen)
• Sensitizing / Priming dose  initial
  contact with allergen
• Shocking dose  2nd contact with same
  allergen  Manifestations of
  Hypersensitivity
• Haptens  Incomplete antigen
Classification
Based on time required               Based on Pathogenesis
• Immediate
   – Anaphylaxis
   – Atopy             I

   – Antibody mediated cell damage
     II

   – Arthus phenomenon
   – Serum sickness         III
• Delayed
   – Infection
   – Contact           IV
Distinguishing features
Immediate                       Delayed
• Appears and recedes rapidly   • Appears slowly and lasts
                                  longer
• Induced by antigens /
                                • Antigen /Hapten intradermally
  haptens by any route            or skin contact
• Circulating antibodies may    • Circulating antibodies need
  be present                      not be present
• Passive transfer possible     • Transfer not possible with
                                  serum but possible with T cells
  with serum                      or transfer factor
• Desensitization easy but      • Desensitization is difficult but
  short lived                     long lasting
Classification
                                     Based on Pathogenesis (Coombs
Based on time required               & Gell)
• Immediate                          • Type I  anaphylactic, IgE
   – Anaphylaxis                       or reagin dependent
   – Atopy             I
                                     • Type II  IgG mediated,
   – Antibody mediated cell damage     rarely IgM
     II
                                     • Type III  immune
   – Arthus phenomenon
                                       complex/ toxic complex
   – Serum sickness         III        disease
• Delayed                            • Type IV  delayed or cell
   – Infection                         mediated immunity
   – Contact           IV
Type 1 Hypersensitivity
• Anaphylaxis
• Atopy
  – Richet
  – Theobald smith theory
Sensitization
• Most effective parentrally but can occur via any route
   – Antigens & Haptens can induce anaphylaxis.
   – Interval of 2-3 weeks is required between priming &
     shocking dose
   – Once sensitized person remains so for a long period
   – Shocking dose is more effective
      •   Intravenous
      •   Intraperitoneally
      •   Subcutaneous
      •   Intradermal
   – Shocking antigen must be identical or immunologically
     identical to sensitizing antigen.
Features of Anaphylaxis
•   Edema
•   Decreased coagulablity of blood
•   Fall in Blood Pressure
•   Fall in temperature
•   Leucopenia
•   Thrombocytopenia
Susceptibility to Anaphylaxis
Anaphylaxis reaction in Humans
• Itching of scalp and tongue
• Flushing of skin all over the body
• Bronchospasm
• Nausea, vomiting, Abdominal pain, Diarrhoea &
  Malena
• A/c Hypotension, loss of consciousness  Death
• Cutaneous Anaphylaxis
    – Small shocking dose  local wheal & flare reaction
    – Used for allergen testing in atopic diseases
• Passive Cutaneous Anaphylaxis
     in vivo method of detection of antibodies
     Intradermal antibody injection to Normal animal
                        4-24 hours
            Antigen + Evan’s Blue

     Immediate blueing at the intradermal site
                    Use
                    To detect human IgG
                    Cannot detect IgE
Mechanism of Type 1 reaction


             B cell to
             plasma
             cell




                         Binding




Activation                         Release
What comes out??
Vasoactive amines   Histamine                Dilatation of blood
                                             vessels
                                             Transient contraction
                                             of smooth muscles
Proteases                                    Local tissue damage
Prostaglandins                               Vascular dilatation
Leukotrienes                                 Prolonged smooth
                                             muscle contraction
Cytokines           IL2, IL3, IL4, IL6, TGF-ß, Local inflammation
                    GM-CSF, IL1 & TNF-α
What comes out?
• Seratonin
• Eosinophil chemotactic factor (ECF-A)
                                           1
• Neutrophil chemotactic factor ( NCF-A)

• Platelet activating factor       2

• Bradykinin
ANAPHYLACTOID REACTIONS

 Peptone , Trypsin etc  anaphylaxis like
  reactions (anaphylactoid reactions)
 No immunological basis

 Non specific mechanisms involving activation
  of complement & release of anaphylotoxins
ATOPY

• Naturally occurring familial hypersensitivities
• Inhalants  Pollens, House dust
• Ingestants  Eggs, Milk
• Contact allergens  antigens not effective
  parenterally but induce IgE formation
• Predisposition to atopy is genetically determined
• Atopy runs in families
• Bottle fed infants tend to develop atopy in later life
IgE
• Intially demonstrated by Radioallergo sorbent test (RAST)
• Now ELISA and Passive agglutination is used
• Prausnitz – kutsner (PK reaction)
       Kustner  atopic to cooked fish
       serum from Kustner

       injected s/c to Prausnitz
                      24hrs
       s/c injection of cooked fish antigen at same site

       wheal & flare reactions in few mins
IgE
• Heat sensitive
• Do not cross placenta
• IgE overproduction  deficiency of IgA  Atopy
• IgE &IgA lymphocytes reside in submucosa
• Antigens are dealt by IgA so IgE never comes into contact
• When IgA is deficient IgE producing cells are exposed  IgE
  overproduction
• Clinically
    –   Eye  conjunctivitis
    –   Respiratory system  Rhinitis
    –   Intestine  G.I Symptoms
    –   Skin  Dermatitis
TYPE II HYPERSENSITIVITY
Type II hypersensitivity

BLOOD TRANSFUSION REACTIONS
HEMOLYTIC DISEASE OF NEWBORN
DRUG INDUCED HEMOLYTIC ANAEMIAS
Blood transfusion reactions
• RBC has a large number                           Mismatched
                                                   transfusion

  of proteins &
  glycoproteins                                Complement
                                               mediated lysis

• Antibodies formed are of
  IgM class                                  Free Hb in plasma

  (Isohemagglutinins)
• Clinically                                  Filtered through
                                                   kidneys

   – Immediate
      • Fever, Chills, Nausea, DIC,
        Low back pain &                       Hemoglobinuria


        Hemoglobin in urine.
   – Delayed                          Hemoglobin                 Bilirubin
Delayed reactions !
• Seen in people with repeated blood transfusions (
  Rh, Kidd, Kell & Duffy)
• Predominant isotype involved is IgG 
  incomplete lysis  RBC destroyed in
  extravascular sites ( Agglutination, Opsonization
  & Subsequent phagocytosis by macrophages)
• Clinically
  – Fever, Low Hb%, Increased Bilirubin, Mild Jaundice.
    Free Hb absent in urine.
Hemolytic disease of Newborn
• Minor
• Serious
• Lethal  Erythroblastosis fetalis

       Hemoglobin
                      Accumulate    Brain
        converted
                        in brain   damage
       to Bilirubin
Hemolytic disease of Newborn
• Prevention
   – Rhogam  antibodies against Rh antigen within 24-48
     hours of delivery
   – Binds to fetal blood cells and clears them before B-cell
     activation and memory cell production.
• Diagnosis
   – Testing of maternal serum for antibodies to Rh antigen.
     Rise in titre is Diagnostic.
   – Presence of maternal IgG on surface of fetal RBC detected
     by coombs test
• Treatment
   – Intrauterine blood exchange transfusion
   – Exposure to U-V light
   – Plasmapheresis to mother
Drug induced Hemolytic anaemia




     Antibiotics attach to RBC

      Drug protein complex

      Formation of antibody

       Bind to drug on RBC

      Activates complement

           Lysis of RBC
Type III Hypersensitivity
• Antigen + Antibody  Immune complex
                        Small                 Large

                  Clearance of antigen    Tissue damage



• Tissue damage                 Localized
                                Generalized
Formed in blood


       Blood vessel wall
     Synovial membrane
Glomerular basement membrane
        Choroid plexus



     Initiates reaction


  Increase in Neutrophils


     Granular release


      Tissue damage
• C3a, C4a & C5a  Anaphylotoxins Local mast cell
  degranulation Increase in local vascular permeability
• C3a, C5a & C5b67  Chemotactic  Attract
  Neutrophils
• Tissue damage is as a result of lytic enzymes by
  neutrophils
• C3b  Opsonin
• Large complexes deposited in basement membrane
• Small complexes deposited in subepithelium
• Phagocytosis unsuccessful as complexes are attached
  to basement membrane  more lytic enzymes poured
  in  membrane attack mechanism of complement 
  destruction of tissue
• Microthrombi formed due to complement induced
  aggregation of platelets & release of clotting factors.
Localized hypersensitivity
                        Increase in
                                              Formation of local   Mediate arthus
  Antigen entry         circulating
                                             immune complexes        reaction
                         antibody




Neutrophils adhere
                                              Localized tissue &   Accumulation of
   to vascular       Reach target site
                                              vascular damage        fluid & RBC
  endothelium




   Pronounced
edema & erythema                      Sensitized individual
  at a faster rate




Intrapulmonary arthus type reactions induced by bacterial spores, Fungi or
dried fecal proteins  Pneumonitis, Alveolitis
Eg-      Farmer’s lung
         Pigeon farmer’s disease
Generalized hypersensitivity
• Large amount of uncleared complexes cause
  reactions at various sites
  – Horse anti tetanus
  – Anti diptheria serum
• Combination of symptoms in patient who has
  received foreign antiserum  Serum sickness
• Clinically  fever, weakness, rash,edema,
  erythema, lymphadenopathy, arthritis,
  Glomerulonephritis
Circulating immune complexes
• Autoimmune
   – Systemic Lupus Erythmatosis
   – Rheumatoid Arthritis
   – Good pastuer’s syndrome
• Drug
   – Penicillins
   – Sulfonamides
• Infections
   –   Post streptococcal glomerulonephritis
   –   Meningitis
   –   Hepatitis
   –   Mononucleosis
   –   Malaria
   –   Trypanosomiasis
Type IV
• Activation of sensitized TDTH Cells  Secretion of
  cytokines  Draws macrophages & activate them
   Promote phagocytosis  Lytic enzymes into
  surrounding tissue  Localized tissue damage.
• Hallmark of type IV
  – Delay in time required for reaction
  – Recruitment of macrophages
• Important defense mechanism against
  intracellular pathogens
Clinical applications
• PPD antigen for detecting previous exposure
  to M.TB
• Lepromin test for leprosy
• Coccidiodin test for coccidiomycosis
• Depletion of CD4+ T cells associated with AIDS
   repeated skin test with various antigens or
  haptens
Contact dermatitis
• Common allergens  Hairdyes, Cosmetics,
  Nickel, Turpentine, Formaldehyde,
  Trinitriophenol,Poison oak, Poison Ivy.
• These complex with skin proteins and internalized
  into APC in skin. These are processed and
  presented to class II MHC  activation of TDTH 
  Release of lymphokines
• Detected by PATCH TEST sensitivity is indicated
  by itching in 4-5hours, Local reactions varying
  from erythema to vesicles to blisters in 24-48
  hours.
CONCLUSION!
References
 Kuby immunology
 Basic immunology – Abbas
Diagnosis
Type 1      Provocation test
            Skin test
            IgE RadioAllergo Sorbent Test (RAST)
            Leukocyte histamine release assay
            Surface markers for basophil activation
            Leukotriene release test
Type 2      IgG Serum test
            (Anti- GBM, Anti Neutrophil cytoplasmic IgG
            Antibody)
Type 3      IgG
Type 4      Skin test
            Lymphocyte transformation test
            MELISA - Memory Lymphocyte Immuno Stimulation
            Assay

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Hypersensitivity

  • 2. I intend to cover in next 30 mins!  Hypersensitivity overview  Classification of hypersensitivity  Type I Hypersensitivity  Anaphylaxis  Atopy  Type II Hypersensitivity  Blood transfusion reactions  Hemolytic disease of newborn  Drug induced hemolysis  Type III Hypersensitivity  Localized  Generalized  Type IV Hypersensitivity  Tuberculin reaction  Contact dermatitis
  • 3. Hypersensitivity • Hypersensitivity is the term used when an immune response results in exaggerated or inappropriate reaction harmful to the host.
  • 4. Hypersensitivity Antigen Immunity • Hypersensitivity is the term used when an Antigen Antigen immune response results in exaggerated killed Host or inappropriate reaction harmful to the host. Antigen ? Hypersensitivity
  • 5. Common terms • Allergen Antigen ( bland substance like serum protein or pollen) • Sensitizing / Priming dose  initial contact with allergen • Shocking dose  2nd contact with same allergen  Manifestations of Hypersensitivity • Haptens  Incomplete antigen
  • 6. Classification Based on time required Based on Pathogenesis • Immediate – Anaphylaxis – Atopy I – Antibody mediated cell damage II – Arthus phenomenon – Serum sickness III • Delayed – Infection – Contact IV
  • 7. Distinguishing features Immediate Delayed • Appears and recedes rapidly • Appears slowly and lasts longer • Induced by antigens / • Antigen /Hapten intradermally haptens by any route or skin contact • Circulating antibodies may • Circulating antibodies need be present not be present • Passive transfer possible • Transfer not possible with serum but possible with T cells with serum or transfer factor • Desensitization easy but • Desensitization is difficult but short lived long lasting
  • 8. Classification Based on Pathogenesis (Coombs Based on time required & Gell) • Immediate • Type I  anaphylactic, IgE – Anaphylaxis or reagin dependent – Atopy I • Type II  IgG mediated, – Antibody mediated cell damage rarely IgM II • Type III  immune – Arthus phenomenon complex/ toxic complex – Serum sickness III disease • Delayed • Type IV  delayed or cell – Infection mediated immunity – Contact IV
  • 9. Type 1 Hypersensitivity • Anaphylaxis • Atopy – Richet – Theobald smith theory
  • 10. Sensitization • Most effective parentrally but can occur via any route – Antigens & Haptens can induce anaphylaxis. – Interval of 2-3 weeks is required between priming & shocking dose – Once sensitized person remains so for a long period – Shocking dose is more effective • Intravenous • Intraperitoneally • Subcutaneous • Intradermal – Shocking antigen must be identical or immunologically identical to sensitizing antigen.
  • 11.
  • 12. Features of Anaphylaxis • Edema • Decreased coagulablity of blood • Fall in Blood Pressure • Fall in temperature • Leucopenia • Thrombocytopenia
  • 14. Anaphylaxis reaction in Humans • Itching of scalp and tongue • Flushing of skin all over the body • Bronchospasm • Nausea, vomiting, Abdominal pain, Diarrhoea & Malena • A/c Hypotension, loss of consciousness  Death • Cutaneous Anaphylaxis – Small shocking dose  local wheal & flare reaction – Used for allergen testing in atopic diseases
  • 15. • Passive Cutaneous Anaphylaxis in vivo method of detection of antibodies Intradermal antibody injection to Normal animal 4-24 hours Antigen + Evan’s Blue Immediate blueing at the intradermal site Use To detect human IgG Cannot detect IgE
  • 16.
  • 17. Mechanism of Type 1 reaction B cell to plasma cell Binding Activation Release
  • 18. What comes out?? Vasoactive amines Histamine Dilatation of blood vessels Transient contraction of smooth muscles Proteases Local tissue damage Prostaglandins Vascular dilatation Leukotrienes Prolonged smooth muscle contraction Cytokines IL2, IL3, IL4, IL6, TGF-ß, Local inflammation GM-CSF, IL1 & TNF-α
  • 19. What comes out? • Seratonin • Eosinophil chemotactic factor (ECF-A) 1 • Neutrophil chemotactic factor ( NCF-A) • Platelet activating factor 2 • Bradykinin
  • 20. ANAPHYLACTOID REACTIONS  Peptone , Trypsin etc  anaphylaxis like reactions (anaphylactoid reactions)  No immunological basis  Non specific mechanisms involving activation of complement & release of anaphylotoxins
  • 21. ATOPY • Naturally occurring familial hypersensitivities • Inhalants  Pollens, House dust • Ingestants  Eggs, Milk • Contact allergens  antigens not effective parenterally but induce IgE formation • Predisposition to atopy is genetically determined • Atopy runs in families • Bottle fed infants tend to develop atopy in later life
  • 22. IgE • Intially demonstrated by Radioallergo sorbent test (RAST) • Now ELISA and Passive agglutination is used • Prausnitz – kutsner (PK reaction) Kustner  atopic to cooked fish serum from Kustner injected s/c to Prausnitz 24hrs s/c injection of cooked fish antigen at same site wheal & flare reactions in few mins
  • 23. IgE • Heat sensitive • Do not cross placenta • IgE overproduction  deficiency of IgA  Atopy • IgE &IgA lymphocytes reside in submucosa • Antigens are dealt by IgA so IgE never comes into contact • When IgA is deficient IgE producing cells are exposed  IgE overproduction • Clinically – Eye  conjunctivitis – Respiratory system  Rhinitis – Intestine  G.I Symptoms – Skin  Dermatitis
  • 25. Type II hypersensitivity BLOOD TRANSFUSION REACTIONS HEMOLYTIC DISEASE OF NEWBORN DRUG INDUCED HEMOLYTIC ANAEMIAS
  • 26. Blood transfusion reactions • RBC has a large number Mismatched transfusion of proteins & glycoproteins Complement mediated lysis • Antibodies formed are of IgM class Free Hb in plasma (Isohemagglutinins) • Clinically Filtered through kidneys – Immediate • Fever, Chills, Nausea, DIC, Low back pain & Hemoglobinuria Hemoglobin in urine. – Delayed Hemoglobin Bilirubin
  • 27. Delayed reactions ! • Seen in people with repeated blood transfusions ( Rh, Kidd, Kell & Duffy) • Predominant isotype involved is IgG  incomplete lysis  RBC destroyed in extravascular sites ( Agglutination, Opsonization & Subsequent phagocytosis by macrophages) • Clinically – Fever, Low Hb%, Increased Bilirubin, Mild Jaundice. Free Hb absent in urine.
  • 28. Hemolytic disease of Newborn • Minor • Serious • Lethal  Erythroblastosis fetalis Hemoglobin Accumulate Brain converted in brain damage to Bilirubin
  • 30. • Prevention – Rhogam  antibodies against Rh antigen within 24-48 hours of delivery – Binds to fetal blood cells and clears them before B-cell activation and memory cell production. • Diagnosis – Testing of maternal serum for antibodies to Rh antigen. Rise in titre is Diagnostic. – Presence of maternal IgG on surface of fetal RBC detected by coombs test • Treatment – Intrauterine blood exchange transfusion – Exposure to U-V light – Plasmapheresis to mother
  • 31. Drug induced Hemolytic anaemia Antibiotics attach to RBC Drug protein complex Formation of antibody Bind to drug on RBC Activates complement Lysis of RBC
  • 33. • Antigen + Antibody  Immune complex Small Large Clearance of antigen Tissue damage • Tissue damage Localized Generalized
  • 34. Formed in blood Blood vessel wall Synovial membrane Glomerular basement membrane Choroid plexus Initiates reaction Increase in Neutrophils Granular release Tissue damage
  • 35. • C3a, C4a & C5a  Anaphylotoxins Local mast cell degranulation Increase in local vascular permeability • C3a, C5a & C5b67  Chemotactic  Attract Neutrophils • Tissue damage is as a result of lytic enzymes by neutrophils • C3b  Opsonin • Large complexes deposited in basement membrane • Small complexes deposited in subepithelium • Phagocytosis unsuccessful as complexes are attached to basement membrane  more lytic enzymes poured in  membrane attack mechanism of complement  destruction of tissue • Microthrombi formed due to complement induced aggregation of platelets & release of clotting factors.
  • 36.
  • 37. Localized hypersensitivity Increase in Formation of local Mediate arthus Antigen entry circulating immune complexes reaction antibody Neutrophils adhere Localized tissue & Accumulation of to vascular Reach target site vascular damage fluid & RBC endothelium Pronounced edema & erythema Sensitized individual at a faster rate Intrapulmonary arthus type reactions induced by bacterial spores, Fungi or dried fecal proteins  Pneumonitis, Alveolitis Eg- Farmer’s lung Pigeon farmer’s disease
  • 38. Generalized hypersensitivity • Large amount of uncleared complexes cause reactions at various sites – Horse anti tetanus – Anti diptheria serum • Combination of symptoms in patient who has received foreign antiserum  Serum sickness • Clinically  fever, weakness, rash,edema, erythema, lymphadenopathy, arthritis, Glomerulonephritis
  • 39. Circulating immune complexes • Autoimmune – Systemic Lupus Erythmatosis – Rheumatoid Arthritis – Good pastuer’s syndrome • Drug – Penicillins – Sulfonamides • Infections – Post streptococcal glomerulonephritis – Meningitis – Hepatitis – Mononucleosis – Malaria – Trypanosomiasis
  • 40.
  • 41. Type IV • Activation of sensitized TDTH Cells  Secretion of cytokines  Draws macrophages & activate them  Promote phagocytosis  Lytic enzymes into surrounding tissue  Localized tissue damage. • Hallmark of type IV – Delay in time required for reaction – Recruitment of macrophages • Important defense mechanism against intracellular pathogens
  • 42. Clinical applications • PPD antigen for detecting previous exposure to M.TB • Lepromin test for leprosy • Coccidiodin test for coccidiomycosis • Depletion of CD4+ T cells associated with AIDS  repeated skin test with various antigens or haptens
  • 43. Contact dermatitis • Common allergens  Hairdyes, Cosmetics, Nickel, Turpentine, Formaldehyde, Trinitriophenol,Poison oak, Poison Ivy. • These complex with skin proteins and internalized into APC in skin. These are processed and presented to class II MHC  activation of TDTH  Release of lymphokines • Detected by PATCH TEST sensitivity is indicated by itching in 4-5hours, Local reactions varying from erythema to vesicles to blisters in 24-48 hours.
  • 45. References  Kuby immunology  Basic immunology – Abbas
  • 46.
  • 47. Diagnosis Type 1 Provocation test Skin test IgE RadioAllergo Sorbent Test (RAST) Leukocyte histamine release assay Surface markers for basophil activation Leukotriene release test Type 2 IgG Serum test (Anti- GBM, Anti Neutrophil cytoplasmic IgG Antibody) Type 3 IgG Type 4 Skin test Lymphocyte transformation test MELISA - Memory Lymphocyte Immuno Stimulation Assay