Immune system

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Immunity are divided into nonspecific immunity and specific immunity. Examples of nonspecific immunity are skin, mucous membrane, and sebum. Specific immunity recognizes and respond to specific foreign substance. Specific immunity are divided into humoral response and cell-mediated response. Humoral response involves the production of antibodies while cell mediated immunity involve the cytotoxic T cells.

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Immune system

  1. 1. IMMUNE SYSTEM•Specific and nonspecific response •Humoral immunity
  2. 2. IMMUNE SYSTEM Pathogen (disease-causing organism) can be bacteria, fungus, virus, or multicellular parasite. Pathogen infects animal because the internal environment of animal offer a suitable habitat. The animal body is the ideal habitat for the pathogen to grow, reproduce, and medium for transportation to the new environments.
  3. 3.  Thus, a defense system must be made up in order to ward off the invasion of pathogen into the animal body. Immune system recognizes the pathogen as foreign body and respond by producing immune cells and protein.
  4. 4. IMMUNITY Immunity is defined as an ability of the body to resist invasion of pathogen or disease. A study of how the immune system of animal works is called immunology. Immunity are divided into nonspecific immunity and specific immunity.
  5. 5. Pathogens (microorganisms and viruses) INNATE IMMUNITY Barrier defenses:Recognition of traits Skinshared by broad ranges Mucous membranesof pathogens, using a Secretionssmall set of receptors Internal defenses: Phagocytic cells Rapid response Antimicrobial proteins Inflammatory response Natural killer cellsACQUIRED IMMUNITY Humoral response:Recognition of traits Antibodies defend againstspecific to particular infection in body fluids.pathogens, using a vastarray of receptors Cell-mediated response: Cytotoxic lymphocytes defend Slower response against infection in body cells.
  6. 6. NONSPECIFIC IMMUNITY Also known as innate immunity. Present before any exposure to pathogens. Act immediately upon infection. Divided into surface barrier and internal defenses.
  7. 7. SURFACE BARRIER Skin is an outer covering of an animal body which act as primary defense system. Possess keratinized epithelial membrane that function as a barrier and prevent the pathogen that swarm on the skin. Keratin is resistant to most weak acids and bases and to bacterial enzymes and toxins.
  8. 8.  Mucous membranes line all body cavities that open to the exterior; the digestive, respiratory, urinary, and reproductive tracts. Epithelial membranes produce a variety of protective chemicals.
  9. 9.  The acidity of skin secretions (pH 3 to 5) inhibits bacterial growth. Sebum contains chemical that are toxic to bacteria. Vaginal secretion of adult females are very acidic. The stomach mucosa, secretes a concentrated hydrochloric acid solution and protein-digesting enzymes.
  10. 10.  Saliva, which cleanses the oral cavity and teeth. Lacrimal fluid of eye contains lysozyme, an enzyme that destroys the bacteria. Sticky mucus traps many microorganisms that enter the digestive and respiratory passageways. Tiny mucus-coated hairs inside the nose traps the pathogen, preventing it from entering the lower respiratory passages.
  11. 11. INTERNAL DEFENSES:CELLS AND CHEMICALS Internal defenses involve phagocytic cells, natural killer cells, antimicrobial proteins, and inflammatory response. The inflammatory response enlists macrophages, mast cells, all types of white blood cells, and other chemicals that kill pathogen. The phagocytic cells are the cells that functions in engulfing the pathogen.
  12. 12. PHAGOCYTIC CELLS If the pathogens succeed to get through the skin, then the phagocytic cells will combat the pathogens. Phagocytic cells consist of monocytes, macrophages, neutrophils and eosinophils. Pathogens are recognized by surface cell receptors which are also known as TLR (Toll-like receptors).
  13. 13. EXTRACELLULAR LipopolysaccharideFLUID Helper TLR4 Flagellin proteinWHITEBLOODCELL TLR5 VESICLE TLR9 TLR3 Inflammatory responses ds RNA
  14. 14.  Macrophages derived from white blood cells, monocytes which leave and enter the tissues, and develop into macrophages. Neutrophils, the most abundant type of white blood cells. Eosinophils, white blood cells that weakly phagocyte the pathogens.
  15. 15. HUMAN LYMPHATIC SYSTEM Interstitial fluid Adenoid Tonsil Lymph Blood nodes capillary Spleen Tissue Lymphatic cells vessel Peyer’s patches (small intestine) Appendix Lymphatic vessels Lymph Masses of node defensive cells
  16. 16. MECHANISM OF PHAGOCYTOSIS Phagocytic cell engulfs the particulate matter. Cytoplasmic extension of phagocyte cell bind to the particulate matter and pull it into vacuole. Phagosome is formed. Phagosome fuses with lysosome, forming a phagolysosome.
  17. 17. MicrobesPHAGOCYTIC CELLVacuole Lysosome containing enzymes
  18. 18. NATURAL KILLER CELLS Function in lysing and killing the cancer cells and virus-infected body cells. Natural killer cells act before the specific immune system is activated. Able to detect and eliminate the virus infected cell and cancerous cell (virus infected cell and cancerous cell do not express class I MHC protein).
  19. 19.  The natural killer cells detect the cell which is lack of self cell surface receptors (class I MHC protein). Natural killer cells also promote the target cells to undergo apoptosis (programmed cell death).
  20. 20. INFLAMMATORY RESPONSE The benefits of inflammatory response:1. Prevent the spread of damaging agents to nearby tissues.2. Disposes of cell debris and pathogen.3. Set the stage for repair (blood clotting).
  21. 21. INFLAMMATORY RESPONSE Factors which elicit inflammatory response:1. Physical trauma ( a blow)2. Intense heat3. Irritating chemicals4. Infection by viruses, fungi, and bacteriaThe four cardinal signs of accute inflammation:1. Pain2. Redness3. Heat4. Swelling
  22. 22. Tissue injured Histamine (released by basophils),chemical mediators, prostaglandin, complement kinin Vasodilation of Increased Attract neutrophils, arterioles capillary monocytes, and•Local hyperemia permeability lymphocytes to(increased blood flow •Capillaries leak injured areato injured area fluid (exudate) (chemotaxis) •Pus formation
  23. 23.  Mast cells- key components of inflammatory response., release histamine. Pus- break down tissue, die or dying neutrophils, dead or living pathogen, accumulate in the wound. Hyperemia (congestion of blood)- causes redness and heat of an inflammed region.
  24. 24.  Inflammation can be divided into local inflammation and systemic inflammation. Fever is an example of systemic inflammation. It is triggered by pyrogens. The high body temperature inhibits the microbial multiplication and enhances body repair.
  25. 25.  Exudates- fluid containing antibodies and clotting factors. Secretion of exudate causes local edema (swelling) and contributes to the sensation of pain.
  26. 26. Splinter Chemical Macrophage FluidMast cell signals Capillary PhagocytosisRed blood cells Phagocytic cell Major events in a local inflammatory responses
  27. 27. INFLAMMATORY CHEMICALSCHEMICAL SOURCE PHYSIOLOGICAL EFFECTSHistamine Granules of basophils and mast cells, released Promotes vasodilation of local in response to mechanical injury, presence of arterioles, increases permeability of certain microorganisms, and chemicals local capillaries, promoting exudate released by neutrophils. formation.Kinins A plasma protein, kininogen is cleaved by the Same as for histamine, also induce enzyme kallikrein found in plasma, urine, chemotaxis of leukocytes and saliva, and lysosomes of neutrophils, and other prompt neutrophils to release types of cells, cleavage releases active kinin lysosomal enzymes, thereby peptides. enhancing generation of of more kinin, induce pain.Prostaglandins Fatty acid molecules produced from Sensitize blood vessels to effects arachidonic acid-found in all cell membranes; of other inflammatory mediators, generated by enzymes of neutrophils, one of the intermediate steps of basophils, mast cells and others. prostaglandin generation produces free radicals, which can cause inflammation; induce pain.
  28. 28. ADAPTIVE/ SPECIFIC IMMUNITY Specific; recognizes and respond to specific pathogens or foreign substances. Systemic; Immunity not only involve to the initial infection site. Possess ‘memory’; Able to mount stronger attacks on the pathogens which encounter the body previously.
  29. 29.  Adaptive immunity are divided into humoral response and cell-mediated response. Humoral response involves the production of antibody. Cell-mediated immunity involves cytotoxic cells.
  30. 30. HUMORAL RESPONSE Antibody-mediated immunity. Production of antibodies by lymphocytes. Antibodies present in the body’s “humors,” or fluids (blood, lymph). Involve antigen recognition, antigen presenting, and B cell proliferation.
  31. 31. B cells undergo maturity (antigen binds to its surface receptor, Tcells nearby) B cells undergo clonal selection (reproduce asexually by mitosis) Plasma cellsAntibodies Long-lived memory cells
  32. 32. Humoral (antibody-mediated) immune response Antigen (1st exposure) Stimulates Engulfed by Gives rise to Antigen- presenting cell B cell Helper T cell Memory Helper T cells Antigen (2nd exposure) Plasma cells Memory B cells Secreted antibodiesDefend against extracellular pathogens
  33. 33. Antigen- presenting cell Peptide antigen Bacterium Class II MHC molecule CD4 TCR (T cell receptor) Humoral Cytokines Helper T cell immunity Cell-mediated(secretion of immunityantibodies by (attack onplasma cells infected cells) B cell Cytotoxic T cell
  34. 34. LYMPHOCYTES (B CELLS AND T CELLS) B cells and T cells are lymphocytes. Involve in the humoral immune response. B cells are originated from the bone marrow. T cells are also originated from the bone marrow but it migrated to the thymus.
  35. 35. ANTIGEN Antigens are foreign substances which elicits adaptive immune response. Antigens are either natural or synthetic. Nonself; antigens are normally not parts of the body. Most antigens are large and complex molecules.
  36. 36.  To elicit adaptive immunity, antigen recognition must occur. Antigen recognition- the B cell and T cell bind to the antigen. The antigen binding- via antigen receptor which attached to the surface of B cell and T cell plasma membranes.
  37. 37. B CELL RECEPTOR Antigen- Antigen- binding site binding Disulfide site bridge V V Variable regions Light C C Constant chain regions Transmembrane region Plasma Heavy chains membrane B cell(a) B cell receptor
  38. 38. T CELL RECEPTOR Antigen- binding site Variable regions V V Constant regions C CTransmembraneregionPlasmamembrane Disulfide bridge Cytoplasm of T cell T cell (b) T cell receptor
  39. 39. B CELLS ANTIGEN RECEPTORSY-shaped.Consist four polypeptide chains. Two identical light chainsand two identical heavy chains.Have constant region (C) and variable region (V).When the antigen receptors bind to an antigen, B cellactivation occurs.
  40. 40.  The antigen receptor bind to the epitope. Epitope- Also known as antigenic determinant, a small, accesible portion of an antigen that binds to an antigen receptor.
  41. 41.  An antigen possesses several different epitopes. All the antigen receptors which are located at a single lymphocyte only bind to the same epitope. When the antigen bind to the antigen receptor, B cell activates and give rise to plasma cells. Plasma cells produce antibodies.
  42. 42. Epitopes (antigenic determinants)Antigen-binding sites Antigen Antibody A Antibody C C C C C Antibody B
  43. 43. ANTIBODIES Also known as immunoglobulins. Similar structure with B cell antigen receptors, but antibodies do not attach to the surface cell membranes.
  44. 44. ANTIBODY CLASSES Antibodies are divided into five major classes. Polyclonal antibodies- products of many different clones of B cells following exposure to a microbial agent. Monoclonal antibodies- prepared a single clone of B cells grown in culture.
  45. 45. Class of Immuno- Distribution Functionglobulin (Antibody IgM First Ig class Promotes neutraliza- (pentamer) produced after tion and cross- initial exposure to linking of antigens; antigen; then its very effective in concentration in complement system the blood activation declines IgG Promotes (monomer) Most abundant Ig opsoniz class in blood; a- also present in tion, tissue fluids neutraliz ation, and cross-linking of crosses placenta, antigens; less thus conferring effec- passive immunity on fetusactivation tive in of IgA Present in Provides localized complement (dimer) secretions such defense of mucous system as tears, saliva, membranes by than IgM mucus, and cross-linking and breast milk neutralization of antigens Triggers release from IgE Present in blood mast cells and (monomer) at low concen- basophils of hista- trations mine and other chemicals that cause allergic reactions IgD (monomer) Present Acts as antigen primari receptor in the ly antigen- on surface of stimulat B cells that have ed not been proliferation and expos differentiation of ed B cells (clonal to antigens selection
  46. 46. Class of Immuno- Distribution Functionglobulin (Antibody) IgM First Ig class Promotes neutraliza- (pentamer) produced after tion and cross- initial exposure to linking of antigens; antigen; then its very effective in concentration in complement system the blood declines activation J chain
  47. 47. Class of Immuno- Distribution Functionglobulin (Antibody) IgG (monomer) Most abundant Ig Promotes opsoniza- class in blood; tion, neutralization, also present in and cross-linking of tissue fluids antigens; less effec- tive in activation of complement system than IgM Only Ig class that crosses placenta, thus conferring passive immunity on fetus
  48. 48. Class of Immuno- Distribution Function globulin (Antibody) IgA (dimer) Present in Provides localized secretions such defense of mucous as tears, saliva, membranes by mucus, and cross-linking and J chain breast milk neutralization of antigens Presence in breast milk confersSecretory passive immunitycomponent on nursing infant
  49. 49. Class of Immuno-globulin (Antibody) Distribution Function IgE Present in blood Triggers release from (monomer) at low concen- mast cells and trations basophils of hista- mine and other chemicals that cause allergic reactions
  50. 50. Class of Immuno- Distribution Function globulin (Antibody) IgD Present primarily Acts as antigen (monomer) on surface of receptor in the B cells that have antigen-stimulated not been exposed proliferation and to antigens differentiation of B cells (clonal selection)Trans-membraneregion
  51. 51. ANTIBODY TARGETS AND FUNCTIONS Neutralization- antibodies block specific sites on viruses or bacterial exotoxins (toxin chemicals secreted by bacteria). The virus or exotoxin cannot bind to the receptors on tissue cells to cause injury.
  52. 52.  Agglutination- Antibodies bind to the antigenic determinant on more on one antigen at a time. Forming antigen-antibody complexes which causes clumping of the foreign cells.
  53. 53.  Precipitation- Soluble molucles are cross-linked into large complexes that settle out of solution.
  54. 54.  Complement fixation and activation- Antibodies bind to cells, cause the antibodies to change its shapes. The antibodies expose the transmembrane regions. Complement fixation into the antigenic cell’s surface is triggered, followed by the cell lysis.
  55. 55. Viral neutralization Opsonization Activation of complement system and pore formation Bacterium Complement proteins Virus Formation of membrane attack complex Macrophage Flow of water and ions Pore Foreign cell
  56. 56. ANTIGEN RECOGNITION B cell antigen receptors – bind to the epitopes of antigens. T cell antigen receptor – bind to the fragments of antigens that are presented on the surface of host cells.
  57. 57. MHC Major Histocompatibility Complex molecule. Encodes a group of glycoproteins called MHC proteins. MHC proteins are divided into two groups, Class I MHC proteins and Class II MHC proteins.
  58. 58. Class I MHC protein Class II MHC proteinFound on virtually all body cells. Found only on certain cells that acts on immune system.Involves in the cell-mediated Involves in the humoral immunity.immunity.
  59. 59. RECOGNITION OF PROTEIN ANTIGENS BY T CELLS The antigen is engulf by the cell. The antigen is cleaved by host cell’s enzyme into antigen fragment. Antigen fragment binds to MHC molecule. Antigen fragment-MHC complex is brought to the surface of the cell. T cell recognizes the antigen fragment-MHC complex.
  60. 60. THE ROLE OF THE MHC Bind to antigen fragment. Transport the antigen fragment to the surface of the cell. Lead to antigen presentation, the display of the antigen fragment on the cell surface.
  61. 61. HELPER T CELLS Activates the adaptive immune response. Antigen fragment is presented by class MHC proteins on the host cell. The host cell which displays the antigen fragment is called antigen-presenting cell.
  62. 62.  In the cell mediated immunity, the Class I MHC protein formed a complex with the antigen fragment. In the humoral immunity, the antigen fragment forms a complex with the Class II MHC protein.
  63. 63. Top view: binding surface exposed to antigen receptors AntigenClass I MHC Antigenmolecule Plasma membrane of infected cell
  64. 64. Antigen-Infected cell Microbe presenting 1. cellAntigen Antigenfragment associat es with Antigen MHC fragmentClass I MHC moleculmolecule e Class II T cell MHC receptor molecule 2. Tcell T cell recognize receptor s combinati a) Cytotoxic T cell on b) Helper T cell
  65. 65. B CELL AND T CELL DEVELOPMENT The antigen presenting leads to B cell and T cell activation. B cell is activated (stimulated to undergo differentiation). B cell proliferates to form clones. The clones bear the same antigen-specific receptors, similar to the activated B lymphocyte cell.
  66. 66.  Some cells from the clones form effector cells.The effector cells which form from the B cells are plasma cells.
  67. 67.  T cell is activated and proliferates to form clones. Some of the clones become effector cells. The effector cells which arise from T cells are divided into helper T cells and cytotoxic T cells.
  68. 68. CLONAL SELECTION The proliferation of B cells is the example of clonal selection process. B cells form clones, a group of cell which are identical to the original cell.
  69. 69. MONOCLONAL ANTIBODY Providing passive immunity. Are made by fusing tumor cells and B lymphocytes. The resulting cell are called hybridomas. Hybridomas proliferates in culture, and produce a single type of antibody. Used to diagnose pregnancy, sexually transmitted diseases, hepatitis and rabies.
  70. 70. CELL MEDIATED IMMUNITY Involve the cytotoxic T cells. Cytotoxic cells- destroy any cells in the body that harbor anything foreign.
  71. 71. Released cytotoxic T cell Cytotoxic T cell Perforin CD8 Dying target cellClass I Granzymes MHC Poremolecule TCRTarge tcell The killing action of cytotoxic T cells
  72. 72. CYTOTOXIC T CELL T cells which undergo proliferation will form effector cells. The effector cells are helper T cells and cytotoxic T cells. The surface of the cytotoxic T cells have glycoproteins called CD8 (different from the helper T cells which possess CD4). All body cells display class I MHC antigens, so all infected cells or abnormal cells can be destroyed by cytotoxic T cells.
  73. 73. Humoral (antibody-mediated) immune response Cell-mediated immune response Antigen (1st exposure) Stimulates Engulfed by Gives rise to Antigen- presenting cell B cell Helper T cell Cytotoxic T cell Overview Memory Helper T cells of acquired/ adaptive Antigen (2nd exposure) Plasma cells Memory B cells Memory Active immune Cytotoxic T cells Cytotoxic T cells system Secreted antibodiesDefend against extracellular pathogens by binding to antigens, Defend against intracellular pathogensthereby neutralizing pathogens or making them better targets and cancer by binding to and lysing thefor phagocytes and complement proteins . infected cells or cancer cells .

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