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Transcript
JS/DipEx 11/16/07 Slide 1 Lecture 11 — Immunology 2 Adaptive immunity Learning Outcomes To b e ab le to: • Humoral responses (B cells) • Cell-mediated responses (T cells) – Specificity – Diversity – Memory – Self-Tolerance 1. outline the principal properties of Adaptive Immunity 2. compare and contrast innate and adaptive immunity 3. explain the principal changes in an immune disorder 4. outline the functions of B cells (incl. immune memory) 5. outline functions of T cells. – Humoral responses (B cells • Immune Disorders – Autoimmune diseases – AIDS Dr Alan Tuffery JS/Dip Ex Tissue Structure — 11 1 Slide 2 Innate vs Adaptive Immunity (reprise) Adaptive Innate (Lymphocytes) (Phagocytosis, Inflammation) • Nonspecific • Specific – Defends against any pathogen upon first exposure – Responds to: – Responds to specific pathogens on 2nd or later exposure • infectious agents • chemical irritants • tissue injury • burns Dr Alan Tuffery – Comes into play after nonspecific responses have begun. JS/Dip Ex Tissue Structure — 11 2 1 JS/DipEx 11/16/07 Slide 3 Features of Adaptive Immunity Specificity Lymphocytes (B and T cells) bind and respond to foreign molecules (antigens) via antigen receptors: each to a specific antigen Diversity The body possesses millions of lymphocytes that can recognise and respond to millions of antigens (one each) Memory 1st exposure to an antigen generates lymphocytes & long-lived memory cells – next exposure to the same antigen, memory cells react more quickly & stronger response (‘acquired immunity’) Self-Tolerance Lymphocytes can distinguish ‘self’ (our normal antigens) from ‘nonself’ (antigens from foreign material). Dr Alan Tuffery JS/Dip Ex Tissue Structure — 11 3 Adaptive Immunity can be NATURAL or ARTIFICIAL Slide 4 Adaptive Immunity Natural Artificial ACTIVE ACTIVE PASSIVE Antibodies are Antibodies or lymphocytes are passed to foetus via placenta produced as a or colostrum result of infection Dr Alan Tuffery PASSIVE Antibodies are Antibodies that produced as a have been produced result of by another animal immunisation or given artificially. with a vaccine JS/Dip Ex Tissue Structure — 11 4 2 JS/DipEx 11/16/07 Slide 5 B Cells — Clonal Selection • Antigen fits B cell’s receptors • Proliferation and differentiation into … 1. Plasma cells • Produce antibodies in blood • (immunoglobulins I gG, IgM, IgE, IgA, I gD) • Short-lived 2. Memory cells (clone) S&G 23.7 (G&S 23.8) Dr Alan Tuffery • With same receptor • Long-lived. JS/Dip Ex Tissue Structure — 11 5 Slide 6 Immune Disorders – Autoimmune Diseases If immune system does not recognise its ‘self’ (e.g. MHC), it reacts against normal cells and tissues DISEASE SYMPTOMS • Systemic lupus erythematosus (SLE) • fever, arthritis, mouth ulcers, etc • Rheumatoid arthritis (RA) • inflammation and damage to the cartilage and bone of joints • Multiple sclerosis (MS) • T cells attack myelin: – (G&S p689) Dr Alan Tuffery Blurred vision, muscle weakness, ataxia. JS/Dip Ex Tissue Structure — 11 6 3 JS/DipEx 11/16/07 Slide 7 Adaptive — Cell-mediated Immunity T cells must S&G 23.10 (G&S 23.11) become activated before they can attack pathogens 1. Cytotoxic T cells The antigen is ‘presented’ by an infected cell via the via its Class I MHC. Dr Alan Tuffery JS/Dip Ex Tissue Structure — 11 7 Slide 8 Adaptive — Cell-mediated Immunity 2. Helper T Cell S&G 23.10 (G&S 23.11) – binds to Class II MHC on an ANTIGEN PRESENTING CELL (e.g. an infected macrophage). Dr Alan Tuffery JS/Dip Ex Tissue Structure — 11 8 4 JS/DipEx 11/16/07 Slide 9 Activated T Cell Responses CYTOTOXIC T CELLS kill infected cells by lysis (direct action) [pic] or apoptosis HELPER T CELLS (~70% of T cells) secrete cytokines that enhance the www.gcarlson.com activity of cytotoxic T cells; enhance phagocytosis stimulate development of B cells into plasma cells (indirect action) SUPPRESSOR T CELLS secrete cytokines that: suppress the activity of B cells, helper, T cells and cytotoxic T cells inhibit phagocytosis. Dr Alan Tuffery JS/Dip Ex Tissue Structure — 11 9 Slide 10 Immune Disorders — Autoimmune Diseases If immune system does not recognise its ‘self’ (e.g. MHC), it reacts against normal cells and tissues DISEASE SYMPTOMS • Systemic lupus erythematosus (SLE) • fever, arthritis, mouth ulcers, • Rheumatoid arthritis (RA) • inflammation and damage to the cartilage and bone of joints • Multiple sclerosis (MS) (p116) • T cells attack myelin: Blurred vision, Muscle weakness, Ataxia Dr Alan Tuffery JS/Dip Ex Tissue Structure — 11 10 5 JS/DipEx 11/16/07 Slide 11 Immune Disorders - AIDS Human Immunodeficiency Virus (HIV) binds to the surface of helper T cells and its nucleic acids (RNA and DNA) enter the T cell Inside the cell, HIV uses the cell to make copies of itself HIV slowly destroys Helper T cells in the body (Helper T cells = 70% of all T cells) When Helper T cell function is impaired, immune responses weaken and other diseases develop. Dr Alan Tuffery JS/Dip Ex Tissue Structure — 11 11 Slide 12 Immune Disorders - AIDS SYMPTOMS HIV Fatigue, fever, swollen glands, headache AIDS Swollen lymph nodes, decreased T cell count; Susceptibility to pneumonia and Kaposi sarcoma; AIDS dementia TRANSMISSION Through blood, semen, vaginal secretions and breast milk Further info (and animations): www.biology.arizona.edu/immunology/tutorials/AIDS/response.html. Dr Alan Tuffery JS/Dip Ex Tissue Structure — 11 12 6 JS/DipEx 11/16/07 Slide 13 Systemic Lupus Erythematosus (SLE) Common Symptoms • Painful or swollen joints and muscle pain • Unexplained fever • Red rashes, mostly in the face • Chest pain upon deep breathing • Unusual loss of hair • Pale or purple fingers or toes from cold or stress (Raynaud's phenomenon) Dr Alan Tuffery • • • • • • • • Sensitivity to the sun Swelling (edema) in legs or around eyes Mouth ulcers Swollen glands Extreme fatigue Anaemia Renal failure Symptoms of lupus can range from mild to severe and may come and go over time. JS/Dip Ex Tissue Structure — 11 13 Slide 14 Learning Outcomes 1 To be able to: 1. outline the principal properties of Adaptive Immunity Specificity, Diversity, Memory, Self-tolerance 2. compare and contrast innate and adaptive immunity Specific — non-specific; 1st — 2nd exposure; fast — slow 3. explain the principal changes in an immune disorder E.g. HIV kills helper T cells — reduced immune competence. Dr Alan Tuffery JS/Dip Ex Tissue Structure — 11 14 7 JS/DipEx 11/16/07 Slide 15 Learning Outcomes 2 To be able to: 4. outline the functions of B cells (incl. immune memory) Produce antibodies (plasma cells); form memory cells 5. outline functions of T cells Cytotoxic T: lyses infected cells Helper T: enhance cytotoxic T, phagocytosis; stim B cells (Ab) Suppressor T: suppress all above. Dr Alan Tuffery JS/Dip Ex Tissue Structure — 11 15 Slide 16 Cell-Mediated Immunity • T cells must become activated before they can attack pathogens • The antigen is ‘presented’ to the T cell by an ANTIGEN PRESENTING CELL (e.g. an infected macrophage) via its MHC. Dr Alan Tuffery www.gcarlsoncom JS/Dip Ex Tissue Structure — 11 16 8