Classification of immune injuries or hypersenstivity reactions or immune reactions


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Classification of immune injuries or hypersenstivity reactions or immune reactions

  1. 1. Classification of Immune Injuries/ Hypersensitivity Allergic Contact Dermatitis Respiratory Allergies Faraza Javed Mphil Pharmacology
  2. 2. Hypersensitivity Hypersensitivity refers to undesirable reactions produced by the normal immune system, including allergies and autoimmunity These reactions may be damaging, uncomfortable, or occasionally fatal.
  3. 3. Classification Type I – Immediate, Atopic, Anaphylactic Type II – Antibody Dependent Type III – Immune Complex Type IV – Cell Mediated / Delayed Type Of Hypersensitivity
  4. 4. TYPE I. Immediate OR Anaphylactic Hypersensitivity  Type I hypersensitivity is also known as immediate or anaphylactic hypersensitivity.  The reaction may involve skin (urticaria and eczema), eyes (conjunctivitis), nasopharynx (rhinorrhea, rhinitis), bronchopulmonary tissues (asthma) and gastrointestinal tract (gastroenteritis).
  5. 5. Mediated by IgE antibody to specific antigens The primary cellular component in this hypersensitivity is the mast cell or basophil. The reaction is amplified and/or modified by platelets, neutrophils and eosinophils.  Mast cells stimulated and release histamine.
  6. 6. Most of the IgE in the body is bound with high affinity receptors (Fc epsilonRI), found on mast cells and basophils. The cells are activated by cross-linking of Fc epsilonRI receptors via antigen binding to the bound IgE molecules.
  7. 7. Such cross-linking leads to rapid degranulation of the mast cells and the release of primary inflammatory mediators stored in the granules. Mast cell activation via Fc epsilonRI also leads to the production of two other types of mediators. These secondary mediators.
  8. 8. Molecules SOME SPACES Effects Primary mediators Histamine Vascular permeability, sm contraction Serotonin vascular permeability, sm contraction Secondary mediators Leukotrienes vascular permeability, sm contraction Prostaglandins vasodilation, sm contraction, platelet activation Bradykinin vascular permeability, sm contraction
  9. 9. Treatment Drugs Non-steroidal anti-inflammatories Antihistamines Steroids Theophylline OR epinephrine -prolongs or increases cAMP levels in mast cells which inhibits degranulation Cromolyn Sodium Prevents release of mediators
  10. 10. Type II Hypersensitivity The second class of damaging reactions is caused by specific antibody binding to cells or tissue antigens. The antibodies are of the IgM or IgG classes and cause cell destruction. It involves binding of antibodies (IgG or IgM) to cell surface antigen or extracellular matrix molecules. Antibody directed to cell surface antigens can activate complement to damage the cells.
  11. 11. Red Blood cell with Ag on cell membrane IgG binds to Ag on membrane Membrane attack complex of compliment lysis red cell (cell death)
  12. 12. The result may be complement mediated lysis as occurs in Haemolytic Anemia ABO Transfusion Reactions. Pencillin allergy also belong to this class.
  13. 13. Type III (Immune-Complex Mediated) Hypersensitivity Due to the formation of antigen-antibody complexes, also called immune- complexes. Type III hypersensitivity is mediated by immune complexes essentially of IgG antibodies. When antibody combines with specific antigen, immune complexes are formed. Normally they are promptly removed by reticulo-endothelial system.
  14. 14. Occasionally, they persist and deposit in tissues resulting in disorders. In persistent microbial or viral infections, immune complexes may be deposited in organs eg. Kidneys - resulting in dysfunction, in joints – arthirits, in BV – Vasculitis. Wherever the immune complexes are deposited, they cause inflammation and tissue injury.
  15. 15. Type IV Hypersensitivity This is the only class of hypersensitive reactions to be triggered by antigen - specific T lymphocyte cells (not antibodies). Cell mediated hypersensivity is induced mainly in skin. When skin again comes in contact with those agents, the sensitized person develops erythema, itching, eczema or necrosis within 12 – 48 hours.
  16. 16.  The Langerhans cell in the epidermis interacts with CD4 T cells to cause contact sensitivity. It occurs after sensitisation with simple chemicals, (e.g nickel & formaldehyde), plant materials (Ivy poison, Oak poison), topically applied drugs (sulfonamides & neomycin), some cosmetics and soaps.
  17. 17. (a) In the sensitization phase after initial contact with antigen (e.g., peptides derived from intracellular bacteria), TH cells proliferate and differentiate into TH1 cells. Cytokines secreted by these T cells are indicated by the dark blue balls.
  18. 18. (b) In the effector phase after subsequent exposure of sensitized TH1 cells to antigen, the TH1 cells secrete a variety of cytokines and chemokines. These factors attract and activate macrophages and other nonspecific inflammatory cells. Activated macrophages are more effective in presenting antigen, thus perpetuating the DTH response, and function as the primary effector cells in this reaction.
  19. 19. A prolonged DTH response can lead to formation of a granuloma, a nodule- like mass. Lytic enzymes released from activated macrophages in a granuloma can cause extensive tissue damage.
  20. 20. Examples Tuberculin response Allergic contact dermatitis Graft rejection Corticosteroids and other immunosuppressive agents are used in treatment.
  21. 21. Comparison of Different Types of hypersensitivity characteris tics type-I anaphylactic type-II (cytotoxic) type-III (immune complex) type-IV (delayed type) antibody IgE IgG, IgM IgG, IgM None antigen exogenous cell surface soluble tissues & organs response time 15-30 minutes minutes-hours 3-8 hours 48-72 hours histology basophils and eosinophil antibody and complement complement and neutrophils monocytes and lymphocytes transferred with antibody antibody antibody T-cells examples allergic asthma, hay fever erythroblastosis fetalis, Goodpasture's nephritis SLE, farmer's lung disease tuberculin test, poison ivy, granuloma
  22. 22. Allergic Contact Dermatitis
  23. 23. Allergic Contact Dermatitis  ACD accounts for approximately 20% of all contact dermatitis ACD is a type IV, delayed or cell-mediated immune reaction that is elicited when the skin comes in contact with a chemical to which an individual has been previously sensitized Synonyms include contact dermatitis and contact eczema
  24. 24. Allergic contact Dermatitis to Leather shoes
  25. 25. Pathogenesis ACD is a type IV hypersensitivity response Requires prior sensitization to the chemical Once sensitized a low concentration of causative chemical elicits a response
  26. 26. Clinical Features of ACD Acute blistering Scaly plaques Patchy and diffuse distributions may be seen with body washes and shampoos
  27. 27. Treatment of ACD Involves identification of causative allergens Clear the dermatitis with topical, or if necessary systemic corticosteroids Complete and prolonged clearing can take up to 6 weeks or more, even when allergens are being avoided
  28. 28. Nickel Most common allergen tested by the NACDG, with 14% of patients Reacting to it. Commonly used in jewelry, Buckles and other metal containing objects.
  29. 29.  Individuals with nickel allergy should avoid custom jewelry and can usually wear stainless steel or gold.
  30. 30. Neomycin Sulphate Most commonly used topical antibiotic used with other antibacterial Agent e.g Bacitracina & Polymixin, as well as Corticosteriods. Co-reactivity is commonly seen with neomycin and bacitracin
  31. 31. Thimerosal Thimerosal is used as a preservative. Most sensitization may be due to its use as a preservative in vaccines. Other exposures include: o Contact lens solution o Otic and opthalmic solutions o Antiseptics and o Cosmetics
  32. 32. Systemic Contact Dermatitis Systemic exposure to a chemical may result in a diffuse dermatitis Patient has had a prior contact allergy and then becomes exposed through a systemic route, such as injection, oral, intravenous, or intranasal administration
  33. 33. One of most common examples is patient with ethylenediamine allergy and Subsequent reaction to aminophylline.
  34. 34. Respiratory Allergies (Allergic Asthma)
  35. 35. Asthma Asthma is a condition characterized by reversible bronchospasm and chronic inflammation of airway passages.
  36. 36. Individuals with asthma appear to produce large amounts of the Antibody IgE that attach to the mast cells present in many tissues. Exposure to a trigger such as pollen will result in the allergen-binding mast cell-bound IgE, which in turn causes the release of inflammatory mediators such as Histamine and Leukotrienes.
  37. 37. The response of a patient with asthma to these triggers can be divided into an ―early phase‖ and a ―late phase.‖
  38. 38. Early Phase of Asthma The early phase of asthma is characterized by: a. Marked constriction of bronchial airways (bronchospasm) b. Difficulty in breathing c. Production of excess mucus. The bronchospasm that occurs may be the result of the increased release of certain inflammatory mediators such as histamine, prostaglandins and bradykinin that, in the early stages of asthmatic response, promote bronchoconstriction rather than inflammation.
  39. 39. Allergen Antigen- presenting cell Processed allergen Plasma Cells IgE antibodies
  40. 40. Early Phase Late Phase Allergen IgE antibodies Inflammation Complications Cellular Infiltration Glands NervesBlood vessels Sneezing Itching Rhinorrhea Congestion Mediator release Eosinophils Basophils Monocytes Lymphocytes Mast cell Irreversible Disease? Priming Hyper- responsiveness Late-phase reaction
  41. 41. Late Phase of Asthma  The late phase of asthma can occur several hours after the initial onset of symptoms and manifests mainly as an inflammatory response.  The primary mediators of inflammation during the asthmatic response are the white blood cells Eosinophils that stimulate mast cell degranulation and release substances that attract other white cells to the area.  Subsequent infiltration of the airway tissues with white blood cells such as Neutrophils and lymphocytes also contributes to the overall inflammatory response of the late phase of asthma.
  42. 42. Some Potential Asthma Triggers.. Allergens — Pollen, pet dander, fungi, dust mites Perfumes Pollutants Cigarette smoke Respiratory tract infections
  43. 43. Sign and Symptoms Early Phase: Shortness of breath Cough Chest tightness and pain Wheezing Cyanosis
  44. 44. Late Phase: Mucosal odema Severe bronchoconstriction Epithelial damage
  45. 45. Staging of Severity Type Day Attacks Night Attacks Mild Intermittant < 2 times in a week < twice in a month Mild Persistant > 2 times in a week > Twice in a month Moderate Persistant > 3 times in a week or Daily > 4 times in a month Severe Persistant Continous or At any time Daily
  46. 46. Treatment Type Quicker Relief Long Term Mild Intermittant Short Acting B2 Agonist Short Acting B2 Agonist Mild Persistant Short Acting B2 Agonist Low Dose Inhaled Steroid OR SR Theophylline OR Leukotriene Antagonist Moderate Persistant Short Acting B2 Agonist High Dose Inhaled Steroid OR Low Dose Inhaled Steroid + Short Acting B2 Agonist
  47. 47. Severe Persistant Short Acting B2 Agonist High Dose Inhaled Steroid + Long Acting Bronchodilators OR SR Theophylline + Oral Prednisolone