1 / 54

Type 4 Hypersensitivity and Autoimmunity Chang Kim

Experts in Clinical ImmunologyOn 4/22/11, all students should present for 5 minutes as if he or she is an expert immunologist on a disease. This presentation accounts for 5% of the final grade.The students should include following components in their presentation:1. What is the immunological mechanism for the disease? Describe the major immune components (cells, cytokines or molecules) and their functions in each disease.2. What are the diagnosis criteria?3. What are the therapy options?.1147

jaden
Download Presentation

Type 4 Hypersensitivity and Autoimmunity Chang Kim

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

    1. Type 4 Hypersensitivity and Autoimmunity Chang Kim

    3. 19. Type IV (Delayed-type or Cell-mediated) Hypersensitivity a. Classification of Type IV reactions: Contact hypersensitivity, tuberculin, NK and T-cytotoxicity, granulomatous b. Contact hypersensitivity (allergic contact dermatitis) (1) Immunologic mechanisms Types of allergens; sensitization and elicitation phases; role of Langerhans cells and keratinocytes; role of antigen-specific TH1 cells and their cytokines; mechanisms of down regulation. (2) Signs, symptoms, incidence and treatment c. Tuberculin-type hypersensitivity (recall response to antigen encountered during infection) (1) Immunologic mechanisms Infections associated with this response; role of antigen-specific TH1 cells and their cytokines; role of macrophages; role of endothelium [adhesion molecule expression and regulation of the influx of cells: PMN first, followed by monocytes and T cells]; macrophages the main cell type; mechanisms of down regulation (e.g. IL10 from macrophages, limited presence of antigen).

    4. Type IV d. TC and NK cell reactions: see previous section on T cell activation and cell mediated immunity e. Granulomatous hypersensitivity (associated with many pathologic effects seen in T cell-mediated immune reactions) (1) Immunologic mechanisms cells: (antigen-specific TH1 cells, macrophages [epithelioid cells, giant cells]) cytokines: IFN-gamma TNF-alpha, IL-3, IL-12, GM-CSF (2) Diseases associated with granulomatous hypersensitivity (brief descriptions) (a) Leprosy (b) Tuberculosis (c) Schistosomiasis (the second most prevalent tropical parasitic disease) (d) Sarcoidosis (A multisystem granulomatous disorder of unknown etiology; involves inflammation that produces tiny lumps of cells in various organs in your body.) (e) Crohn's disease (f) Hypersensitivity pneumonitis (early form involves Type III; an inflammation in the lungs caused by exposure to an (foreign substance), usually organic dust) f. Evaluation of DTH (1) Patch test (to help determine the contactant) (2) Skin test to evaluate CMI (injection of an antigen to see if this is a reactant; e.g. a tuberculin skin test for tuberculosis)

    5. Classification of Hypersensitivity Reactions

    6. Figure 10-36

    9. Figure 10-35

    11. Figure 10-2

    14. 20. Autoimmunity and autoimmune diseases a. Origins of autoimmune diseases (1) Genetic factors: familial incidence; association with specific HLA (or MHC) haplotypes (2) Failure to maintain self-tolerance (either central or peripheral) (3) Loss of regulatory T cells (dysregulation of the cytokine network) (4) Expression of cryptic self epitopes (5) Inappropriate expression of MHC II molecules or co-receptors on specific tissue (6) Cross-reacting antigens and antigenic mimicry (7) Polyclonal B cell activation (8) Association of certain infectious diseases with the onset of autoimmunity (9) Hormonal influences

    15. Pathogenic mechanisms of autoimmune diseases (see individual diseases) c. Examples of autoimmune diseases (prevalence, signs, symptoms, pathologic consequences of autoimmune mechanisms, examples of treatments [some key features of the diseases are given below])

    16. Figure 11-17

    17. Figure 11-37

    21. Figure 11-19

    22. Mutations in the T cell transcription regulator FOXP3 FOXP3 is expressed by “regulatory T cells (Tregs)” FOXP3 is essential for generation of Tregs. Tregs suppress the activation of other immune cells.

    24. Figure 11-23

    27. Figure 11-28

    29. Figure 11-31Figure 11-31 part 2 of 2

    30. Figure 11-30

    31. Figure 11-32

    32. Figure 11-2

    33. Immune Thrombocytopenic Purpura (ITP) Antibodies attach to blood platelet, cells that help stop bleeding, and cause their destruction. Thrombocytopenia refers to decrease in blood platelet. Purpura refers to the purplish-looking areas of the skin and mucous membranes (such as the lining of the mouth) where bleeding has occurred as a result of decreased platelet. Some cases of ITP are caused by drugs, and others are associated with infection, pregnancy, or immune disorders such as systemic lupus erythematosus. About half of all cases are classified as "idiopathic," meaning the cause is unknown.

    38. Figure 11-5

    40. Figure 11-6

    42. (3) Autoimmune Liver and Gastrointestinal Diseases Inflammatory Bowel Disease: Crohn's Disease (abnormality of mucosal T cell regulation; granulomatous reaction characteristic); Ulcerative colitis (Possibly Type II; continuous mucosal ulceration common) Pernicious Anemia (antiparietal cell antibodies and anti-intrinsic factor antibodies) A chronic illness caused by impaired absorption of vitamin B-12 because of a lack of intrinsic factor (IF, transporter of V.B12) in gastric secretions. V.B-12 is a component of an enzyme required for thymine synthesis. (c) Autoimmune Chronic Active Hepatitis (HLA-B8/DR3; liver cells express MHC II proteins; anti-liver cell antibodies are present)

    44. Figure 11-11

    47. Figure 11-12

    50. Autoimmune Neurologic Diseases (a) Multiple Sclerosis (abnormal T cell regulation; Type II and IV; inflammatory demyelination in CNS white matter resulting in "plaques"; auto-antibodies to MBP and PLP of myelin) (b) Acute Disseminated Encephalomyelitis (follows infection or vaccination; Type IV directed at MBP and other myelin antigens) (c) Acute Inflammatory Polyneuropathy (Guillain-Barre’ Syndrome; follows viral or Campylobacter infection; Type II and IV reaction to peripheral nerve antigens) (d) Myasthenia gravis (Type II autoimmune; Abs directed at acetylcholine receptors)

    54. Figure 11-1 part 1 of 3

    55. Figure 11-1 part 2 of 3

More Related