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Overview of the immune system

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Overview of the immune system

  1. 1. Overview of the Immune System Prepared by: Dr. Ami B. Naik Assistant Professor CGBIBT, Uka Tarsadia University
  2. 2. Immunity  Immunity is body's ability to resist or eliminate potentially harmful foreign materials or abnormal cells.
  3. 3. Immunity 1.Immunity: : Meaning the state of protection from infectious disease. 2. Agents: microorganisms (viruses, bacteria etc) and their products, foods, chemicals, pollen, tumor cells, etc. 3.Immune system: immune tissues and organs, immune cells, immune molecules 4.Immune response: collective and coordinated response to the introduction of foreign substances. 5.Immunology: study the structure of immune system and its functions.
  4. 4. Consists of following activities ◦ Defense against invading pathogens (viruses & bacteria) ◦ Removal of 'worn-out' cells (e.g., old RBCs) & tissue debris (e.g., from injury or disease) ◦ Identification & destruction of abnormal or mutant cells (primary defense against cancer) ◦ Rejection of 'foreign' cells (e.g., organ transplant) ◦ Inappropriate responses:  Allergies - response to normally harmless substances  Autoimmune diseases
  5. 5. Brief History of Immunology  1. Empirical Immunology (AD1700-1900)  2. Scientific Immunology (1900-1950s)  3. Modern Immunology (1960s-Present)
  6. 6. History  Discipline of immunology grew out of observation that individuals who recovered from infectious diseases and protected from disease.  430 BC  phenomenon of immunity can be traced back to Thucydides, the great historian of the Peloponnesian War.- plague in Athens.  Recovered from plague and nurse others.  After 2000 years concept recognized.  15th Century  Chinese and Turks tried to prevent smallpox  Dried crust from pustules were inhaled or inserted into small cuts  Variolation  1718  Lady Montagu had that technique done in her children
  7. 7. Documents show that as early as AD 1000, the ancient Chinese custom existed of having children inhale powders made from the crusty skin lesions of patients recovering from smallpox
  8. 8. History  1798 ◦ Edward Jenner  Noticed that milkmaids that contracted cowpox were immune to smallpox  Innoculated small boy with fluid from cowpox pustule  He then intentionally infected the boy with smallpox – the child did not develop smallpox  Lack of disease target and knowledge of their cause.  Technique applied to other disease after ~100 years.  1881 ◦ Louis Pasteur  Cholera and chicken--- Vaccine  Vaccinated sheep with heat-attenuated anthrax  Then infected sheep with virulent strain of anthrax – they did not develop anthrax and non vaccinated, died.
  9. 9. Edward Jenner (1749-1823) Jenner vaccination
  10. 10.  Lious Pasteur (1822~1895).  The genius of Pasteur carried him to the solution of many problems: the spoilage of beers and wines, with the accompanying pasteurization process; the discovery of anaerobic bacteria, virus vaccines, and attenuation of virulence; and studies of spontaneous generation.  His studies in immunology have rightly earned him the position
  11. 11. History  1883  Metchnikoff demonstrated that certain white blood cells were able to phagocytes microorganisms
  12. 12.  Elie Metchnikoff (1845~1916)  He shared the Nobel Prize with Ehrlich in 1908.
  13. 13.  Paul Ehrlich (1854~1915).  He shared the Nobel Prize with Metchnikoff in 1908.  Selective theories(Paul Ehrlich,1900)  The binding like the fitting of a lock with key, the side- chain specificity was determined before its exposure to Ag, and the Ag selected the appropriate side-chain receptor.
  14. 14.  Around 1900,  Jules Bordet at the Pasteur Institute expanded the concept of immunity by demonstrating specific immune reactivity to nonpathogenic substances, such as red blood cells from other species.  Serum from an animal inoculated previously with material that did not cause infection would react with this material in a specific manner, and this reactivity could be passed to other animals by transferring serum from the first.
  15. 15.  1901 ◦ Von Behring and Kitasato  Demonstrated that serum (noncellular component of blood) from animals, immunized to diptheria could transfer that immunity to non- immunized animals.
  16. 16.  1930s,  Through the efforts of Elvin Kabat, a fraction of serum first called gamma-globulin (now immunoglobulin) was shown to be responsible for all these activities.  The active molecules in the immunoglobulin fraction are called antibodies.  In due course, a controversy developed between those who held to the concept of humoral immunity and those who agreed with Metchnikoff ’s concept of cell-mediated immunity.  Immunity requires both cellular and humoral responses.
  17. 17.  1940s,  Merrill Chase succeeded in transferring immunity against the tuberculosis organism by transferring white blood cells between guinea pigs. This demonstration helped to rekindle interest in cellular immunity.  With the emergence of improved cell culture techniques in the 1950s, lymphocyte was identified as the cell responsible for both cellular and humoral immunity
  18. 18. 1930s and 1940s  Instructional Theory, challenged selective theory.  Antigen would be served as template where, antibody would fold.  Antibody is a configuration complementary to antigen.  Postulated by Friedrich Breinl and Felix Haurowitz in 1930 and redefined by Linus Pauling in 1940 in terms of protien folding.
  19. 19. Clonal selection theory and immune tolerance
  20. 20. The clonal selection hypothesis
  21. 21. MHC
  22. 22. Monoclonal Ab and Immune regulatory theories
  23. 23. Susumu Tonegawa is a Japanese Scientist who won the Nobel Prize for physiology or medicine in 1987 "for his discovery of the genetic principle for generation of antibody diversity" Antibody Diversity
  24. 24. Peter C. Doherty Rolf M. Zinkernagel ”for their discoveries concerning the specificity of the cell mediated immune defence”
  25. 25. The Nobel Prize in Physiology or Medicine 2011 was divided, one half jointly to Bruce A. Beutler and Jules A. Hoffmann "for their discoveries concerning the activation of innate immunity" and the other half to Ralph M. Steinman "for his discovery of the dendritic cell and its role in adaptive immunity".
  26. 26. Overview of the Immune System Immune System Innate (Nonspecific) 1o line of defense Adaptive (Specific) 2o line of defense
  27. 27. Innate Immunity Adaptive Immunity
  28. 28. 29  The innate immune response is essential for elimination of a pathogen but not sufficient.  The adaptive immune response requires certain key players of the innate immune response to become activated.
  29. 29. Herd immunity  Herd immunity (or community immunity) occurs when a high percentage of the community is immune to a disease (through vaccination and/or prior illness), making the spread of this disease from person to person unlikely.  Even individuals not vaccinated (such as newborns and the immunocompromised) are offered some protection because the disease has little opportunity to spread within the community.
  30. 30. Innate immune system: components of Blood Complement proteinsCoagulation proteins Cyto kines WBCs Extracellular
  31. 31. White blood cells (WBCs) Macrophages B-lymphocytes T-lymphocytes Natural killer(NK) cells Mast cells
  32. 32. Neutrophils in innate immune response  Most abundant WBCs (~50-60%)  Efficient phagocytes  Most important cells of the innate immune system
  33. 33. Phagocytosis  Phago = to eat  Cyte = cell  WBCs (eg. Neutrophils) – find, eat and digest microbes !
  34. 34. How do neutrophils eat and digest microbes ? Granule s
  35. 35. What’s in the granules ? Lysozyme – digests bacterial cell wall; other antimicrobial proteins
  36. 36. Additional role of neutrophils Triggers inflammatory response
  37. 37. Monocytes  Monocytes (~5% of WBCs)  Migrate into the tissues and become Macrophages Lung Bone Liver Brain intestine
  38. 38. Macrophages  “Big eaters”  Phagocytosis of microbes in tissue (Neutrophils are present only in blood)  Antigen presentation
  39. 39. Natural killer cells  Not B-lymphocytes / T- lymphocytes  Important part of the innate immune system  Kill virus /bacteria infected cells (Intracellular pathogens)  Kills cancer cells
  40. 40. NK cells differentiate choose cells to kill ? Uninfected cell / Normal cell Microbe infected cell / cancer cell Some cell surface proteins are miss
  41. 41. How does the killer kill ? Kills both host cells and microbe Release of granules with perforins and proteases
  42. 42. Defense Against Disease If these barriers are penetrated, the body responds with If the innate immune response is insufficient, the body responds with Adaptive Immune Response cell-mediated immunity, humoral immunity Nonspecific External Barriers skin, mucous membranes Innate Immune Response phagocytic and natural killer cells, inflammation, fever
  43. 43. First line of defense  Non-specific defenses are designed to prevent infections by viruses and bacteria. These include: ◦ Intact skin ◦ Mucus and Cilia ◦ Phagocytes
  44. 44. Role of skin  Dead skin cells are constantly sloughed off, making it hard for invading bacteria to colonize.  Sweat and oils contain anti-microbial chemicals, including some antibiotics.
  45. 45. Role of mucus and cilia  Mucus contains lysozymes, enzymes that destroy bacterial cell walls.  The normal flow of mucus washes bacteria and viruses off of mucus membranes.  Cilia in the respiratory tract move mucus out of the lungs to keep bacteria and viruses out.
  46. 46. Role of phagocytes  Phagocytes are several types of white blood cells (including macrophages and neutrophils) that seek and destroy invaders.  Some also destroy damaged body cells.  Phagocytes are attracted by an inflammatory response of damaged cells.
  47. 47. Role of inflammation  Inflammation is signaled by mast cells, which release histamine.  Histamine causes fluids to collect around an injury to dilute toxins. This causes swelling.  The temperature of the tissues may rise, which can kill temperature-sensitive microbes.
  48. 48. Role of fever  Fever is a defense mechanism that can destroy many types of microbes.  Fever also helps fight viral infections by increasing interferon production.  While high fevers can be dangerous, some doctors recommend letting low fevers run their course without taking aspirin or ibuprofen.
  49. 49. Specific defenses  Specific defenses are those that give us immunity to certain diseases.  In specific defenses, the immune system forms a chemical “memory” of the invading microbe.  If the microbe is encountered again, the body reacts so quickly that few or no symptoms are felt.
  50. 50. Major players  The major players in the immune system include: ◦ Macrophage ◦ T cells (helper, cytotoxic, memory) ◦ B cells (plasma, memory) ◦ Antibodies
  51. 51. Some vocabulary:  Antibody: a protein produced by the human immune system to tag and destroy invasive microbes.  Antibiotic: various chemicals produced by certain soil microbes that are toxic to many bacteria. Some we use as medicines.  Antigen: any protein that our immune system uses to recognize “self” vs. “not self.”
  52. 52. Antibodies  Antibodies are assembled out of protein chains.  There are many different chains that the immune system assembles in different ways to make different antibodies.
  53. 53. Antibodies as Receptors  Antibodies can attach to B cells, and serve to recognize foreign antigens.
  54. 54. Antigens as Effectors  Free antibodies can bind to antigens, which “tags” the antigen for the immune system to attack and destroy.
  55. 55. Antigen recognition  Cells of the immune system are “trained” to recognize “self” proteins vs. “not self” proteins.  If an antigen (“not self”) protein is encountered by a macrophage, it will bring the protein to a helper T-cell for identification.  If the helper T-cell recognizes the protein as “not self,” it will launch an immune
  56. 56. T cells ◦ Arise in bone marrow but mature in thymus ◦ 2 well define subpopulations of T cells  T helper cells  T cytotoxic cells
  57. 57.  T cells  Cytokines secreted by TH cells can activate phagocytic cells  TC cells can kill altered self-cells  Cells infected by viruses  Tumor cells
  58. 58. B cells  B-cells in general produce antibodies.  Those with antibodies that bind with the invader’s antigen are stimulated to reproduce rapidly.  B-cells differentiate into either plasma cells or memory B-cells.  Plasma cells rapidly produce antibodies.  Memory cells retain the “memory” of the invader and remain ready to divide rapidly if an invasion occurs again.
  59. 59. Clonal Selection
  60. 60. Role of antibodies  Antibodies released into the blood stream will bind to the antigens that they are specific for.  Antibodies may disable some microbes, or cause them to stick together (agglutinate). They “tag” microbes so that the microbes are quickly recognized by various white blood cells.
  61. 61. “Killer” T cells  While B-cells divide and differentiate, so do T-cells.  Some T-cells become cytotoxic, or “killer” T-cells. These T-cells seek out and destroy any antigens in the system, and destroy microbes “tagged” by antibodies.  Some cytotoxic T-cells can recognize and destroy cancer cells.
  62. 62. Adaptive Immunity  Antigenic specificity  Diversity  Immunologic memory  Self/nonself recognition
  63. 63. B Lymphocyte
  64. 64. T Lymphocyte