Hypersensitivity seminar.ppt

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  • 2. IMMUNOPATHOLOGY 0 Defects or malfunction in either innate or acquired immune response provokes the illness or disease. 0 Overactive immune response-Hypersensitivity 0 Inappropriate reaction to self-autoimmunity 0 Ineffective immune response-immunodeficiency
  • 3. HYPERSENSITIVITY 0 Undesired immune response 0 Hypersensitivity is a state existing in a previously sensitized individual which leads to tissue damage on later exposure to the allergen. 0 It depends on the individual.
  • 4. HISTORY 0 2000 years ago, Lucretius states that “Differences are so great that one man’s meat is another man’s poison”. 0 Paul Poiter and Charles Richet- Pysalia the jelly fish- aqueous glycine extract administered to 5 dogs but they didn’t die. But after the second dose immediately reacted with illness, vomiting, diarrhea, asphyxia and died within few minutes. 0 Hence they coined this overreaction as anaphylaxis. 0 Awarded Noble Prize in physiology or medicine in 1913 .
  • 5. 0 1st exposure-sensitization 0 2nd exposure- shocking dose 0 Anaphylaxis- without protection rather than an anamnestic (non forgetting) protective response. 0 Anaphylaxis : 0 humoral immunity – immediate hypersensitivity 0 Cell- mediated immunity – delayed-type hypersensitivity.
  • 6. CAUSES OF HP DISEASES 0 Reaction against environmental antigens – production of IgE antibodies cause allergic reactions. 0 Reaction against microbes 0 Autoimmunity
  • 7. CLASSIFICATION OF HYPERSENSITIVITY 0 In 1960s Gell and Coombs classified it into 4 types . 0 Type I – Immediate anaphylaxis 0 Type II – antibody – dependent cytotoxic hypersensitivity 0 Type III – Immune complex-mediated cytotoxicity 0 Type IV – delayed type hypersensitivity
  • 8. TYPE I HYPERSENSITIVITY 0 CHARACTERISTICS: 0 occur quickly after 2nd exposure to the antigen or allergen 0 Inflammation reaction consists of accumulation of basophils, eosinophils, neutrophils, Th2 cells 0 IgE mediated response 0 Antigens – plants, foods, drugs, insect products, mold spores, animal hair, foreign serum, vaccines 0 Atopy:the genetic predisposition to synthesize inappropriate levels of IgE specific for external allergens
  • 10. Slow reacting substance of anaphylaxis
  • 11. Degranulate and release the biological mediators Preformed granule mediators Histamine New generated mediators Bradykinin Leukotrienes Platelet activating factor Prostaglandin D2 Dilate capillaries,increase permeability, increase mucus secretion, contract smooth muscle Systemic anaphylaxis Skin Respiratory tract Degist tract
  • 12. Treat target organs Drug therapy: sodium chromoglcate-stabilize PM & inhibit degranulation Antihistamine & acetyl salicylic acid
  • 13. TYPE II HYPERSENSITIVITY 0 CHARACTERISTICS: 0 Antibody dependent cell-mediated cytotoxicity (ADCC) 0 Antibody (IgM & IgG) activate the complement system which lyse the cell and destroy it.
  • 15. Allergen Stimulate Antibody Cell A. Opsonic phagocytosis Combined opsonic activities D. ADCC of NK C. Effect of complement Cell injury ways of type II hypersensitivity
  • 16. Antigen or hapten on cell Antibody (IgG, IgM) Activate complement Lyse target cell Opsonic phagocytosis Destroy target cell Target cell injury NK , phagocyte Stimulate / block ADCC Change the function ofTarget cell Mechanism of Type II hypersensitivity
  • 18. TYPE III
  • 19. TYPE III Free Ag + Primed Ab Larger immune complex Deposit in tissue or blood vessel wall Inflammation
  • 20. 2、Mechanism of type III hypersensitivity Formation of the intermediate immune complex Deposition of the intermediate immune complex Tissue injury by the immune complex
  • 21. Soluble antigen Body Antibody Immune complex Small molecular soluble Immune complex intermediate molecular soluble Immune complex Large molecular insoluble Immune complex Deposit on the basement of capillariesEliminate by phogacytosis Combine and activate complement system Basophils and mast cells C3a,C5a,C3b Platelets Infiltration of neutrophils Release of vasoactive amine Blood Clotting Mechanisms Phagocytose complex Release of vasoactive amine Aggregation of platlets Release the enzymes in lysosome Increase vascular permeability Edema Tissue injury Thrombus Increase vascular permeability Bleeding Local or systemic immune complex diseases Edema
  • 22. 3. common disease of type III hypersensitivity 1. Local immune complex disease Arthus reaction :Experimental local reaction, Necrotic vasculitis vasculitis, Ulcer Human local reaction: insulin-dependent diabetes mellitus (IDDM) 2. Acute systemic immune complex disease serum sickness Anti-serum Ab+Ag systemic tissue injury ,fever, arthritis, skin rash Pinicillin、Sulfanilamide Acute immune complex glomerulonephritis : Streptococcus infection 3. Chronic immune complex disease SLE Rheumatoid arthritis :RF+IgG Deposit on synovial membrane
  • 23. 5. Type IV hypersensitivity 1、characteristics of type IV hepersensitivity 2、 mechanism of type IV hepersensitivity 3、common diseases of type IV hepersensitivity
  • 24. 1. Characteristics Interaction of primed T cells and associated antigen Infiltration of Mononuclear Cells, Inflammatory response
  • 25. 2. Mechanism of type IV hypersensitivity Formation of effector and memory T cells Inflammation and cytotoxicity caused by effector T cells 1) Inflammation and tissue injury mediated by CD4+Th1 Release chemokines and cytokines Immune injury mainly caused by infiltration of mononuclear cells and lymphocytes 2) Cytotoxicity of CD8+CTL
  • 26. Antigen Induce T cell (CD4+,CD8+) CD4+ T cell Release Secondary contact Primed T cell CD8+ T cell Cytokines IL-2 TNF-b INF-g TF MCF MIF MAF SRF Infiltration of monocyte and Mf Proliferation of T cell Exudation and edema Cytotoxicity Directly kill target cells Inflammation characterized by infiltration of Mf , monocyte, And tissue injury Mechanism of type IV hypersensitivity
  • 27. 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
  • 28. SUMMERY
  • 29. THANK YOU……..
  • 30. 0 0 0 0 0 0 0 0 Immunopathology, diagnosis, and management of hypersensitivity pneumonitis. Abstract Hypersensitivity pneumonitis (HP) is an inflammatory interstitial lung disease caused by a wide variety of organic particles and certain small-molecular weight chemical compounds that provoke an exaggerated immune response in susceptible individuals. The clinical manifestations are heterogeneous and have been classically described as acute, subacute and chronic. The chronic form has an insidious onset over a period of months or years, with progressive dyspnea and often evolves to fibrosis. The pathology is characterized by a bronchiolocentric interstitial mononuclear cell infiltration, nonnecrotizing poorly formed granulomas, cellular pneumonitis and variable degrees of fibrosis. However, morphological diagnosis of HP is complicated because the subacute/chronic forms may be difficult to distinguish from idiopathic pulmonary fibrosis/usual interstitial pneumonia and nonspecific interstitial pneumonia. In general, diagnosis of HP represents a challenge for clinicians that need to weigh a constellation of clinical, laboratory, radiographic and (when available) pathological evidence for each patient to assess the certainty of the diagnosis. The cornerstone of therapy is antigen avoidance. Although clinical trials are scanty, corticosteroids are usually indicated based upon expert opinion. In this review we summarize the current evidence regarding the diagnostic criteria and therapeutic strategies as well as the immunopathological mechanisms putatively implicated in the development of the disease. Arch Pathol Lab Med. 2008 Feb;132(2):204-5. doi: 10.1043/1543-2165(2008)132[204:HPAIR]2.0.CO;2. Hypersensitivity pneumonitis: an immunopathology review. Woda BA. Source Department of Pathology, University of Massachusetts Medical School, Worcester, USA. wodab@ummhc.org