Vertebrate Immunity PDF

Topic 3 Vertebrate Immunity 24-25 Syllabus Assessments Lesson 1 & 2 – Pathogens, & Transmission What is a pathogen? Any micro-organism that will negatively affect an organism it enters. (Cause harm) Can you think of any examples? Transmission of communicable d...

Topic 3 Vertebrate Immunity 24-25 Syllabus Assessments Lesson 1 & 2 – Pathogens, & Transmission What is a pathogen? Any micro-organism that will negatively affect an organism it enters. (Cause harm) Can you think of any examples? Transmission of communicable diseases  http://images.slideplayer.com/9/2540200/slides/slide_19.jpg Challenge: Are there any differences in how the diseases in plants are transmitted and how the diseases in animals are What is direct transmission? http://classconnection.s3.amazonaws.com/921/flashcards/2753921/jpg/direct_contact1360549930141.jpg Can you give some examples of direct transmission in animals?   Amoebic dysentry What is indirect transmission? Can you think of some examples of indirect transmission in animals? Staphylococcus infections Gas gangrene  Vectors – Indirect Transmission in Animals Modern day bubonic plague victim Transmission between animals and humans Factors affecting transmission of communicable diseases in animals Culture and Overcrowded living/ infrastructur Socio-economic working conditions e factors e.g. lack of trained health workers Climate change What increases the probability of catching a communicable disease? Poor nutrition Poor waste disposal A compromised immune system STARTER Primary- non specific defence mechanisms Primary Defences 1. A protective covering – skin 2. Epithelia covered in mucous 3. HCl in the stomach 4. Sweat, tears, urine and saliva contain lysozyme 5. Expulsive reflexes – coughs and sneezes, vomiting, diarrhoea 6. Ear canal lined with wax to trap pathogens 7. Mucus plug in the cervix protects female reproductive system 8. Inflammation 9. Blood clotting and skin repair  MUCOUS MEMBRANES  SKIN SKIN continued…  Animal Defenses. (Flow Chart) Phagocytes, a type of white blood Pathogen is Pathogen gains cell that engulfs pathogens. Antigen blocked by entry to the body. Presenting cells take the pathogen physical to inactivated T-Helper Cells. defences. Antibodies T-Helper Cells become activated & differentiate. B-Plasma Cell T-Helper Cell Unactivated B- T-Memory Cell B-Effector Cells T-Regulator Cell Cell T-Killer Cell B-Memory Cell Animal Defenses, Pre-invasion Just like a castle, your body prevents invaders from invading. (In this case, pathogens!) Here is a brief list of the physical defences your body uses; The Skin! Mucuous Membranes (lining of the respiratory tract) Lysozymes in tears & urine. Also, coughing & sneezing. Blood clots & repair of wounds. Our bodies suffer from a lot of wear & tear. Should we cause enough damage to breach the skin, the body works to close it up as quickly as it can, & prevent infection. You need to know about this process. (Next slide.) BLOOD CLOTTING https://www.youtube.com/watch?v=PjhHQHMnMjI SKIN REPAIR INFLAMMATORY RESPONSE Mast cells Histamine Cytokines Phagocytes Vasodilation Blood vessels Permeable Tissue fluid Swelling Redness Pain Heat  INFLAMMATORY RESPONSE Localised response to pathogens resulting in inflammation at the site of the wound Pain, heat, redness and swelling Mast cells activated, which release chemicals called histamines and cytokines Histamines – make the blood vessels dilate and become more permeable, causing localised heat and redness. The raised temperature helps prevent pathogens reproducing Histamines – make blood vessels more leaky so blood plasma is forced out, once forced out of the blood it is known as tissue fluid. Tissue fluid causes swelling (oedema) and pain Excess tissue fluid is drained in to the lymphatic system where lymphocytes are stored – this can lead to pathogens coming in to contact with he lymphocytes and initiating specific immune responses (more on this later) Cytokines – attract white blood cells to the site. They dispose of the pathogens by phagocytosis L3 – Secondary non-specific defences   Phagocytes Secondary Defence (non specific) Neutrophils and Monocytes - Phagocytosis  NEUTROPHILS MONOCYTES STRUCTURE WHERE ARE Stem cells in the bone Stem cells in the bone THEY MADE? marrow marrow DIAPEDESIS (can Yes Yes squeeze out of capillaries) MISCELLANEOUS Abundant in blood Short-lived Circulate the blood (macrophages as they leave the Contain a large number of blood) lysosomes. Settle in tissues where Released in large numbers as a infection is more likely – lungs, result of infection. gut, liver Usually die soon after digesting Longer life a few pathogens, collect in Play a role in initiating the infected area to form pus. specific responses to invading pathogens Antigen- presenting cells NEUTROPHIL OR MACROPHAGE? Phagocytosis Phagocytosis Lysosome contains powerful hydrolytic Pathogen is surrounded Phagocytic vesicle enzymes by cell extensions and engulfed/phagocytosed Lysosome fuses with the phagocytic Waste is removed by Contents of the vesicle reverse phagocytosis phagocytic vesicle are digested or exocytosis  Antigen Presenting Cells (APCs) Fevers – Non-Specific Immunity SUMMARY QUESTIONS Lesson 4 – Non Specific Immune System – Cell Research Choose cells from the following list, research their structure, and their roles within the immune response. Also – note down anything they do that is bad for the organism. Lesson 5 – Activating T Cells & The MHC 1. 2. 3. 4. 5.  Animal Defenses. (Flow Chart) Phagocytes, a type of white blood Pathogen is Pathogen gains cell engulf the pathogen. Antigen blocked by entry to the body. Presenting cells take the pathogen physical to inactivated T-Helper Cells. defences. Antibodies T-Helper Cells become activated & differentiate. B-Plasma Cell T-Helper Cell Unactivated B- T-Memory Cell B-Effector Cells T-Regulator Cell Cell T-Killer Cell B-Memory Cell Activating T Cells. While in the thymus, the developing T cells start to express T cell receptors (TCRs) and other receptors called CD4 and CD8 receptors. All T cells express T cell receptors, and either CD4 or CD8, not both. So, some T cells will express CD4, and others will express CD8. Unlike antibodies, which can bind to antigens directly, T cell receptors can only recognize antigens that are bound to certain receptor molecules, called Major Histocompatibility Complex class 1 (MHCI) and class 2 (MHCII). These MHC molecules are membrane-bound surface receptors on antigen-presenting cells, like dendritic cells and macrophages. CD4 and CD8 play a role in T cell recognition and activation by binding to either MHCI or MHCII. What is the MHC? – Info not available in textbooks. use the link below. Antigen presentation by major histocompatibility complex (MHC) proteins is essential for adaptive immunity. Prior to presentation, peptides need to be generated from proteins that are either produced by the cell’s own translational machinery or that are funneled into the endo- lysosomal vesicular system. The prolonged interaction between a T cell receptor and specific pMHC complexes, after an extensive search process in secondary lymphatic organs, eventually triggers T cells to proliferate and to mount a specific cellular immune response. What is the MHC? – Info not available in textbooks. use the link below. What is the MHC? – Info not available in textbooks. use the link below. Many T Cells, Each With A Different Receptor For Antigens…   T-Helper Cells become activated & differentiate. T-Helper Cell T-Regulator Cell CD4+ Receptors. They take the CD4+ & T-Killer Cell antigens from T-Memory Cell CD25+. These the APC and go kill off other T to activate a B Remains in the cells when CD8+ Receptors. Cell in the bone body for years, if there are no These are activated marrow. the antigen is found more PAMPS. & go to the site of again in the body, infection & attack any the response time is infected area. quicker. Lesson 6 – March Of The B Cells Learning Outcomes:  Lymphocytes Secondary defence - specific Hardly any cytoplasm Originate from stem cells in the bone marrow Spherical nucleus  2 TYPES B CELLS T CELLS Mature in Bone marrow Mature in Thymus Gland MIGRATE MIGRATE Lymph nodes, Lymph nodes, spleen, spleen, adenoids, tonsils, adenoids, tonsils, blood, blood, lymphatic system lymphatic system B and T lymphocytes B lymphocytes T lymphocytes ▪ When activated secrete ▪ Either regulate activity antibody against specific of other cells of the antigens immune system ▪ Can encounter antigen in ▪ Or, kill virus infected blood or on the plasma cells directly membrane of an APC. ▪ Can only respond to their antigen if they find it in the plasma membrane of another cell B lymphocytes (B cells) - Humoral Quick Research:  The selected lymphocyte divides repeatedly to produce a clone Some of the Some of the clone clone become become memory antibody- cells that can secreting plasma respond rapidly to a cells future infection Plasma cells secrete antibody Memory cells for future use New encounter Plasma cells secrete antibody Memory cells for future use 1. 2. THE MAIN FUNCTION OF B CELLS IS TO…  Lesson 7: Antibodies KEY DEFINITIONS ANTIGEN ANTIBODY IMMUNE RESPONSE  Antigens http://www.proniquescientific.com/Antigens.png Antibodies Hinge region gives flexibility in binding to antigen Hinge region Disulphide bridges Chain of sugar molecules ANTIBODIES AND ANTIGENS :match them up correctly? The structure of an antibody Antibody functions Consequences of antibody binding Consequences of antibody binding Antibodies Enhances activity of macrophages, acts as antitoxins and causes agglutination Causes agglutination Inhibits bacteria Involved in response to sticking to host cells infections and allergic or forming colonies on responses mucous membranes Immune responses http://images.tutorvista.com/content/immune-system/antigen-antibodies-formation.jpeg Lesson 8: Vaccinations and Immunity Types of immunity Natural immunity Artificial immunity Passive immunity Active immunity What is natural passive immunity? Natural passive immunity occurs when an individual receives antibodies from their mother via: *The placenta as a foetus. * The mother’s milk during suckling - The milk formed from the breasts of the mother during the first few days after birth contains antibodies. This early milk, called colostrum, has a high concentration of antibodies which remain in the intestines and are absorbed into the blood providing temporary immunity to a variety of pathogens. What is artificial passive immunity? Artificial passive immunity occurs when antibodies from another individual are injected. This takes place in the treatment of diseases such as tetanus and diphtheria. What is natural active immunity? Natural active immunity results from an individual becoming infected with a disease under normal circumstances. The body produces its own antibodies, and may continue to do so for many years. It is for this reason that many people suffer from diseases such as measles only once in a lifetime. The immunity results from the activities of B lymphocyte memory cells. What is artificial active immunity? Artificial active immunity forms the basis of immunisation. It involves inducing an immune response in an individual without them suffering the symptoms of the disease. This is achieved by introducing the appropriate disease antigens into the body, either by injection or by mouth. The process is called vaccination, and the material introduced is called a vaccine. What is a vaccine made from? There are different forms of vaccine: Living attenuated microorganisms are living microorganisms which have been treated, e.g. by heat, so that they do not cause symptoms, but still multiply. Although harmless, they stimulate the body’s immune system. Measles, tetanus and poliomyelitis can be vaccinated against in this way. Dead microorganisms have been killed by some means. Again, they are harmless, but induce immunity. Typhoid, cholera and whooping cough can be controlled by this means. Genetically engineered microorganisms can be produced in which the genes for antigen production are transferred from a harmful organism to a harmless one. These are then grown in fermenters and the extracted antigen is separated and purified before injection. Hepatitis B vaccine is one of this type.  Natural Artificial Inherited or acquired Acquired deliberately by naturally, not deliberately exposure to causative agent Passive Antibodies pass from Antibodies from a different Results from the mother individual or organism are introduction of antibodies To foetus via placenta injected from another organism’s To baby during suckling immune system, rather than one’s own Short lived Active Antibodies acquired as a Antigens are injected or Results from the activities of result of a previous given by mouth as a an individual’s own immune infection producing B vaccine. They induce the system lymphocyte memory cells, body to produce is own Long lasting which are reactivated on antibodies to the disease. the second infection Vaccine may contain Dead pathogen Attenuated pathogen Genetically engineered antigens Features of a successful vaccination programme – A suitable vaccine – Few, if any, side effects – The mechanisms to produce, store and transport the vaccine – The means of administering the vaccine properly at the appropriate time. – The ability to vaccinate the vast majority (all, if possible) of the vulnerable population herd immunity Lesson 9: Autoimmune Disorders Student Disorder Researched Autoimmune Disorders Criteria Below! Produce an overview of the disorder as well as any known causes (genetic otherwise) State what type of leukocyte causes the autoimmune disorder (is involved in recognizing self as non-self & do they harm the cell.) What cell is attacked/damaged by the autoimmune disorder. What symptoms are caused by the disorder? Are there any currently available treatments? Are there any treatments currently being researched?