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Immune System

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  • 1. Immune System
  • 2. Introduction • An animal must defend itself against pathogens (organism or virus that causes a disease) – Viruses – Bacteria – Fungi – Parasites • Protozoa –heterotrophic protists (eukaryotes, usually unicellular); giardia, trypanosoma, plasmodium (malaria) • Worms (flatworms & roundworms) – Prions
  • 3. 3 Types of Defense Fig. 43.1 Nonspecific: doesn’t distinguish one pathogen from another Specific: recognition of a pathogen by lymphocytes; development of immunity Copyright © 2002 Pearson Education, Inc., publishing as Benjamin Cummings
  • 4. 1st Line of Defense: Nonspecific Skin, Mucous Membranes, Secretions
  • 5. Physical barriers: skin & mucous membranes • Mucus: viscous fluid secreted by cells of mucous membranes, traps microbes and other particles • Washing: tears, saliva, sweat Chemical barriers: • Stomach acid: kills most pathogens, but not all (ie. giardia, hep A) • Skin secretions: from sebaceous and sweat glands in skin – pH 3-5 to prevent colonization of microbes – lysozymes: antimicrobial enzymes, digest cell walls of bacteria
  • 6. 2nd Line of Defense: Nonspecific Inflammatory Response & Phagocytosis
  • 7. Tissue damage leads to: • Inflammatory Response: enhanced blood flow and vessel permeability  characteristic swelling, redness, and heat of inflammation • Phagocytosis: ingestion of pathogens by phagocytes (leukocytes/WBCs)
  • 8. Systemic Inflammatory Response Severe tissue damage or infection  widespread response – Rapid increase in leukocytes in the blood within a few hours after the initial events – Fever can be triggered by toxins from pathogens or by pyrogens released by certain leukocytes – Inhibits growth of some microbes, facilitating phagocytosis, and speeding up tissue repair Septic shock: characterized by high fever and low blood pressure; most common cause of death in U.S. critical care units
  • 9. Localized Inflammatory Response Fig. 43.5 1. Damaged cells release chem signals (histamine, prostaglandins) 2. Nearby capillaries dilate & become more permeable; fluid and clotting agents move from the blood to the site 3. Chemokines & other chemotactic factors attract phagocytes from the blood 4. Phagocytes consume pathogens & cell debris, producing pus Copyright © 2002 Pearson Education, Inc., publishing as Benjamin Cummings
  • 10. Blood Clotting: prevention of blood loss, pathogens from entering Fig. 42.16 Copyright © 2002 Pearson Education, Inc., publishing as Benjamin Cummings
  • 11. Blood clotting steps 1. Endothelium of blood vessel is damaged and connective tissue is exposed to blood 2. Platelets (cell fragments) adhere to collagen fibers (glycoprotein in the extracellular matrix; nonelastic; does not tear easily) in connective tissue 3. Platelets and tissue release chemicals that makes nearby platelets sticky 4. Platelets form a ‘plug’ that provides emergency protection against blood loss 5. When vessel damage is more severe, a clot of fibrin reinforces this ‘plug’
  • 12. Fibrinogen  Fibrin Fibrinogen: ‘inactive’ soluble plasma protein Fibrin: ‘active’ insoluble plasma protein clotting factors released from clumped platelets or damaged cells + clotting factors in blood plasma prothrombin  thrombin (inactive plasma protein) (an active enzyme) thrombin catalyzes the conversion of fibrinogen (soluble)  fibrin (insoluble) fibrin threads get woven into a ‘patch’
  • 13. Red blood cells trapped in a clot of fibrin http://media-2.web.britannica.com/eb-media/28/98328-004-5514AFAC.jpg
  • 14. Phagocytosis: ingestion of pathogens by phagocytes (leukocytes/WBCs) http://www.textbookofbacteriology.net/Phago.jpeg
  • 15. Phagocytes 1. Neutrophils 2. Monocytes 3. Eosinophils
  • 16. Neutrophils • 60%-70% of leukocytes (WBCs) • damaged cells (by invading pathogens) release chemical signals (cytokines) that attract neutrophils from the blood • neutrophils enter infected tissue, engulfing and destroying pathogens by • self-destruct as they destroy foreign invaders • avg life span = days http://education.vetmed.vt.edu/Curriculum/VM8054/Labs/Lab6/IMAGES/Neutrophil%20Blood%20WITH%20LABEL%20copy.jpg
  • 17. Monocytes • 5% of WBCs • more effective than neutrophils • circulate in blood a few hours • then migrate into tissues and develop into macrophages macrophages: large, long-lived phagocytes • avg. life span = months (macrophages) Locations of macrophages: - circulate in body: blood & lymph - tissues: lung, liver, kidney, connective tissue, brain, lymph nodes, spleen Fig. 43.3: phagocytosis by a macrophage Copyright © 2002 Pearson Education, Inc., publishing as Benjamin Cummings
  • 18. Lymphatic system Fig. 43.4a Copyright © 2002 Pearson Education, Inc., publishing as Benjamin Cummings
  • 19. Eosinophils • 1.5% of WBCs • large parasitic invaders (ie blood fluke, Schistosoma mansoni) • position themselves against external wall of a parasite, discharge destructive enzymes from cytoplasmic granules http://www.funsci.com/fun3_en/blood/blood_09.gif
  • 20. NOT Phagocytes: Natural Killer (NK) cells (but part of the nonspecific response) • destroy virus-infected body cells • also attack abnormal body cells that could become cancerous • NOT phagocytic: mount an attack on the cell’s membrane, causing the cell to lyse A natural killer cell (NK cell, yellow) of the immune cell attacking a cancer cell (red). http://www.bio-pro.de/imperia/md/images/artikelgebunden/stern/nk_tumor_338x319.jpg
  • 21. 3rd Line of Defense: Specific Immunity T cell B cell http://www.besthealth.com/besthealth/bodyguide/reftext/im ages/tcell.jpg http://www.biooncology.com/bioonc/images/b-cell-lg.jpg
  • 22. Specific immunity: lymphocytes (leukocytes) recognize and respond to particular foreign bodies by generating selective immunity responses throughout the body  specificity
  • 23. Antigens Antigen: a foreign ‘invader’ (pathogens, transplanted cells, cancer cells) that elicits a specific response by lymphocytes (T cells & B cells) – Each antigen has a particular molecular shape – Stimulates B cells to secrete antibodies antibody generator Antigen receptors: membrane proteins on lymphocytes responsible for recognizing antigens B cell: immunoglobulins T cell: T cell receptors
  • 24. 1. Lymphocytes
  • 25. 2 main types of lymphocytes: B lymphocytes (B cells) T lymphocytes (T cells) – both circulate throughout the blood and lymph – concentrated in the spleen, lymph nodes, & other lymphatic tissue – specialize in recognizing different types of antigens – carry out specific defensive actions that complement each other
  • 26. All lymphocytes come from stem cells B cells remain and mature in the bone marrow T cells migrate from the bone marrow & develop in the thymus Fig. 43.8 Copyright © 2002 Pearson Education, Inc., publishing as Benjamin Cummings
  • 27. 2. Immune Responses
  • 28. Immunity Antibodies: proteins produced by B cells that function as ‘effectors’ of an immune response; produced in humoral response/clonal selection; responsible for immunity Challenge and response: immunity to a disease is only developed if the immune system is challenged by the disease
  • 29. Types of Immunity Humoral Cell-Mediated bacteria, toxins, viruses bacteria, viruses, fungi, in protozoa, parasitic blood plasma & lymph worms, cancer (body fluids) in cells B cells T cells
  • 30. Overview of immune response http://library.thinkquest.org/03oct/01254/images/immune_map.jpg
  • 31. Macrophage engulfs pathogen, presents antigen for immune response
  • 32. Cell Mediated Cytotoxic (Killer) Helper T cells T cells • Cancer • produce cytokines • viruses • phagocytosis • inflammatory response • B cells • Memory T cells http://library.thinkquest.org/03oct/00520/home.html
  • 33. Humoral B cell with antibodies Helper T cell antigen activated B cell proliferate lots of activated B cells plasma cells memory B cells antibodies  find/attach to pathogens phagocytosis http://library.thinkquest.org/03oct/00520/home.html
  • 34. Clonal Selection: antigen-driven cloning of lymphocytes
  • 35. Active vs Passive Immunity Active immunity: immunological memory is developed by the immune system when exposed to an antigen • Natural: the body actively produces antibodies after being exposed to an infectious disease • Artificial: vaccination (also called immunization) = antigens transferred into an individual
  • 36. Vaccination • Vaccine: inactivated, killed, parts (proteins), viable but weakened (attenuated) • No longer cause disease, but they can act as antigens, stimulating an immune response and immunological memory • Examples: flu, yellow fever, hepatitis A & B
  • 37. Immunological Memory in Vaccination Fig. 43.7 Copyright © 2002 Pearson Education, Inc., publishing as Benjamin Cummings
  • 38. Active vs passive immunity (cont.) Passive immunity: antibodies are transferred from one individual to another; only temporary b/c immune system has not developed immunological memory • Natural: antibodies are transferred from a pregnant mother to her fetus (blood) and from a nursing mother to an infant (breast milk) • Artificial: antibodies from an animal already immune to a disease are transferred via blood transfusion or injection (ie snake antivenin)
  • 39. Monoclonal Antibodies • antibodies specific for one antigen • production – Isolation & purification of an antigen – Injection of antigen into healthy animal – Immune system stimulated to form activated plasma cells which produce antibodies – Plasma cells extracted and cultured with cancer cells – Plasma/cancer cell hybridomas which survive for long periods of time and produce lots of antibodies
  • 40. Monoclonal antibodies (cont.) • diagnostic tests – target antigen identification: antibodies detect and mark antigens; signals are sent; Western Blot, ELIZA • colorimetric – enzymes • chemiluminescent agents • radioactive labels • Fluorescent labels – gonorrhea, HIV, Lyme disease
  • 41. Monoclonal antibodies (cont.) • Treatment – cancer • attach to cancer cell antigens, causes immune response; Rituximab (B cell non-Hodgkin lymphoma, CD20 antigen) • Stops cancer cells from growing by blocking cell surface protein activation – autoimmune disorders (i.e. MS) – delivery of medicine
  • 42. Aquired ImmunoDeficiency Syndrome • In U.S., late 1970s/early 1980s, increased rate of Kaposi’s sarcoma & pneumonia in homosexual men, hemopheliacs, blood transfusion recipients, children of these gps • Symptoms: opportunistic infections (pulmonary, gastrointestinal), cancer (Kaposi’s sarcoma, lymphoma), neurological disorders (encephalopathy), fevers, sweats, weight loss • Almost 100% mortality; most lethal pathogen ever
  • 43. Karposi’s Sarcoma is a symptom of AIDS
  • 44. Human ImmunoVirus http://www.stanford.edu/group/virus/retro/2005gongishmail/hiv1.jpg
  • 45. HIV (cont.) • Retrovirus: RNA virus transcribes RNA into DNA; retro = backwards • 2 major strains: HIV-1 & HIV-2 • Infects CD4 cell surface proteins on T helper cells, macrophages, some lymphocytes, some brain cells • Transmission: via genital or colonic mucosa during sexual intercourse; blood to blood contact; breast milk Did you know condoms (when used correctly) are 99% effective?!!
  • 46. For HIV/AIDS, you need to research: • Global & local social implications • Global & local economic implications • Transmissions • Prevention