1. Chapter 22: The Lymphatic System Primary sources for figures and content: Marieb, E. N. Human Anatomy & Physiology. 6 th ed. San Francisco: Pearson Benjamin Cummings, 2004. Martini, F. H. Fundamentals of Anatomy & Physiology. 6 th ed. San Francisco: Pearson Benjamin Cummings, 2004.

2. Lymphatic System Functions 1.Reclaim lost fluid for return to cardiovascular system 2.Protect against pathogens & cancer cells -Nonspecific defenses: general protection -Does not distinguish threat specifics -Specific defenses: immune response -Identify and defend against one particular threat Immunity = resistance to infection through activation of specific defenses

3. Lymphatic System Components 1.Lymph: -Fluid similar to plasma but less proteins 2.Lymphatic vessels: -Carry lymph from tissues to veins 3.Lymphoid tissues and organs: -site of development of lymphocytes and screening for pathogens 4.Lymphocytes and Phagocytes: -provide defense

4. Lymphocyte Production Lymphocytes are produced: –in lymphoid tissues (e.g., tonsils) –lymphoid organs (e.g., spleen, thymus) –and in red bone marrow

5. The Circulation of Fluids From blood plasma to lymph and back to the venous system Also transports hormones, nutrients, and waste products

6. Lymph and Lymphatic Vessels Lymph originates as fluid lost from blood capillaries Fluid collected in blind end lymphatic capillaries Endothelial cells loosely bound together with overlap acts as one-way valve: –allows fluids, solutes, viruses, and bacteria to enter –prevents return to intercellular space Fluid, solutes, large objects driven into lymphatic capillary by pressure in interstitial space

7. Figure 22–2 Lymphatic Capillaries

8. Figure 22–3 Lymphatic Vessels and Valves

9. Lymphatic Vessels Histologically most like veins All three tunics Large ones have vasa vasorum Many valves Many anastomoses Lymph nodes present along vessels

10. Lymph nodes http://howshealth.com/lymph-node-cancer/

11. Lymphatic Vessels Converge, return fluid to blood stream: Lymphatic capillaries  lymphatic collecting vessels  lymphatic trunks  subclavian veins

12. Lymphangitis Inflammation of a lymphatic vessel Cause: –Toxins or infection Symptom: –Vasa vasorum swell with blood due to pressure Clinical sign: –Appears as red line under skin

13. Lymphoid Cells 1.Macrophages: -Phagocytosis and T cell activation 2.Dendritic cells: -Antigen presentation (found in CT) 3.Lymphocytes: -Constantly circulate between blood, lymph, tissues -Can survive 20+ years -3 classes: -T cells, B cells, and Natural Killer cells

14. The importance of lymphocytes, and how are they distributed in the body.

15. 3 Classes of Lymphocytes 1.T cells -“Thymus dependent”, 80% -Cytotoxic T cells: cell mediated immunity -kill “foreign” cells and viruses directly -Helper T cells: activate T & B cells -Suppressor T cells: inhibit T & B cells

16. 3 Classes of Lymphocytes 2.B cells -“Bone marrow derived, 10-15% -Antibody mediated or humoral immunity -When activated  plasma cells  secretes antibodies (immunoglobin proteins)  antibodies bind specific antigens (Targets which identify any pathogen or foreign compound)

17. 3 Classes of Lymphocytes 3.Natural Killer Cell -5-10% -Nonspecific defense -Attack abnormal cells -Cancer cells or virus-infected cells

18. Figure 22–5 Production of Lymphocytes: Lymphopoiesis

19. Occurs in bone marrow, thymus, and lymphoid tissues Hemocytoblast  lymphoid stem cell –One type of lymphoid stem cell stays in bone marrow  produce B cell and NK cells –One type migrates to thymus  produce T cells Both B and T cells –can divide to produce more of the same type (clones) –Can migrate to all lymphoid tissues for division and development

20. Lymphoid Tissue Reticular CT, lymphocytes, and other lymphoid cells Function 1.Proliferation site for lymphocytes 2.Surveillance point for lymphocytes and macrophages Two types of Lymphoid Tissue 1. Lymphoid follicles/nodules 2. Lymphoid organs

21. 1. Lymphoid Follicles/Nodules CT packed with lymphocytes –T, B, and dendritic cells No capsule Germinal center middle with dividing B cells Germinal center is surrounded by dendritic cells, T cells and some macrophages Follicles associated with respiratory, digestive, and urinary tracts Special lymphoid nodules: –MALT, Appendix, Tonsils

22. 1. Lymphoid Follicles/Nodules Special lymphoid nodule/follicle collection 1.MALT (mucosa-associated lymphoid tissue) -Deep to intestinal epithelium -Made up of individual nodules called Peyer’s Patches 2.Appendix -Tubular offshoot of beginning portion of large intestines

23. 1. Lymphoid Follicles/Nodules 3.Tonsils -Large nodules in pharynx, have crypts to trap bacteria  encourage development of immunity -5 Total: -2 palatine tonsils -1 pharyngeal (adenoid) -2 lingual tonsils

24. http://antranik.org/the-immune-system/

25. Figure 22–6 Lymphoid Nodules

26. Lymphoid Organs Have fibrous CT capsule around outside Contain many lymphoid follicles Include: 1. Lymph nodes 2. Thymus 3. Spleen

27. 1. Lymph Nodes -Bean shaped, 1-25 mm -Have associated blood vessels and nerves

28. 1. Lymph Node Structure -Capsule = CT, surrounds outside -Trabeculae = folds of capsule creating partitions inside -Cortex = outer edge -Superficial cortex = lymphoid follicles with B cells and dendritic cells -Deep cortex = T cells, transit between lymph and blood -Medulla = center, houses T, B and plasma cells -Sinuses = spaces throughout that house macrophages -Allow lymph flow through node

29. Figure 22–7 1. Lymph Nodes

30. Lymph Flow Through Node 1.Lymph enters via many afferent vessels – from peripheral tissues to lymph node 2. Flows slowly through sinuses where it is surveyed for pathogens and antigens –Macrophages engulf pathogens –Dendritic cells bind antigens and stimulate lymphocytes 3. “clean” lymph exits via few efferent vessels that carry lymph to venous circulation *Lymph nodes clustered mostly along lymphatic trunks, nodes function to purify lymph before returning it to blood

31. Figure 22–1

32. If pathogen detected in Node 1.Pathogen detected -antigens are “presented” to lymphocytes to stimulate lymphocytes 2. Lymphocytes increase in number –Rapid clonal division of B & T cells 3. Causes node to swell = buboes –Yersinia pestis  Bubonic plague

33. Lymph node Diseases Lymphadenopathy –Chronic enlargement of lymph nodes, due to infection or cancer Cancer often metastasizes in lymph vessels –Blood capillaries restrict access of cells but lymphatic capillaries do not

34. 2. Thymus T cells mature in cortex and migrate to medulla to enter blood Thymus produces hormones –Thymosin & Thymopoietin Both promote development and maturation of lymphocytes, mostly the T cells in thymus Thymus most active in early childhood Thymus atrophies with age

35. Figure 22–8 2. The Thymus

36. 3. Spleen Located lateral to stomach Function: –Remove abnormal blood cells –Store iron from recycled RBCs for reuse –Initiate immune response by B & T cells in response to antigens in blood –Store platelets –Site of fetal erythrocyte production

37. 3. Spleen Structure: –Red pulp Sinusoids filled with RBCs, platelets, and macrophages which phagocytose old RBCs and pathogens –White pulp Lymphoid follicles containing lymphocytes, await antigen to activate

38. Figure 22–9 3. The Spleen

39. 3. Spleen Spleen cleans blood –Blood flows slowly through sinusoids –Macrophages and lymphocytes detect and destroy foreign cells and antigens Spleen = mostly sinusoids –Bleeds profusely when damaged –To fragile to stitch tears –Splenectomy to prevent fatal hemorrhaging –Liver and bone marrow can take over functions

40. How would blockage of the thoracic duct affect the circulation of lymph? A.It would prevent drainage from the left arm. B.It would prevent drainage from the lower appendages. C.It would cause lymphedema. D.All of the above.

41. If the thymus failed to produce thymic hormones, which population of lymphocytes would be affected? A.B lymphocytes B.T lymphocytes C.monocytes D.antigen-producing cells

42. Why do lymph nodes enlarge during some infections? A.Because there is a bacterial invasion of the node. B.Due to phagocytic and lymphatic cell division. C.Due to accumulation of antibodies. D.Due to accumulation of circulating T cells.

43. Body Defenses Against Pathogens Provide resistance to fight infection, illness, and disease 2 categories of defenses: –nonspecific defenses –specific defenses

44. Three Lines of Defense 1 st line: prevent entry  skin & mucosa 2 nd line: general antimicrobial actions when first line has been penetrated -Nonspecific defense = innate defense 3 rd line: precision assault on a specific pathogen -Specific defense = immune response

45. The body’s nonspecific defenses and their functions.

46. Nonspecific Defenses Always work the same way Against any type of invading agent Born with it

47. Figure 22–10 7 Nonspecific Defenses Skin, hair, secretions macrophages, neutrophils, eosinophils NK cells antiviral chemicals antibacterial proteins restrict spread of injury accelerate metabolism

48. 7 Types of Nonspecific Resistance 1.Physical barriers 2.Phagocytic cells 3.Immunological surveillance 4.Interferons 5.Complement 6.Inflammation 7.Fever

49. 1. Physical Barriers 1.Cutaneous Membrane (skin): -Impenetrable layers of keratinized cells -Impermeable to water and chemicals -Acid pH due to sebum -High salt due to perspiration -Acid and salt inhibit microbial growth 2.Mucosa: -Produces antimicrobial secretions: -Acid  inhibit microbe growth -Lysozyme  lyse bacterial cell walls -Mucus  traps microbes

50. 2. Phagocytes 1.Microphages (neutrophils & eosinophils) -Either phagocytose pathogens OR -Secrete defensins on pathogen -Defensins cause membrane pores that result in lysis of target cell 2.Macrophages -Phagocytose pathogens, cell debris and foreign material -Fixed macrophages  Non-traveling, associated with specific tissues or organs (e.g. microglia) -Free macrophages  Travel throughout body via blood

51. 2. Phagocytes All Phagocytes: –Emigrate from capillaries –Display chemotaxis –Have receptors to bind target for phagocytosis

52. 2. Phagocytosis 1.Phagocytic cell adheres to target via receptors 2.Pseudopods from around target to engulf 3.Target internalized in phagosome  fused with lysosome 4.Target digested in phagolysosome: -Small solutes diffuse into cytoplasm for use -amino acids, glucose, etc. -Undigestable = residual body 5.Enzymes neutralized and residual body is exocytosed

53. 2. Phagocytosis

54. 3. Immunological Surveillance Means monitoring of tissues by NK cells for abnormal cells (cancer or virus infected) 1. Abnormal cells express abnormal antigens on the surface  detected by NK cells 2. NK cell binds abnormal cell and releases perforins from Golgi 3. Perforins assemble on target membrane creating pores  lysis of target

55. Figure 22–11 Natural Killer Cell Function

56. 4. Interferons Means: 1.Antiviral cytokines -Cytokines = chemicals used for cell to cell communication 2.Proteins released by activated lymphocytes, macrophages, or virus- infected cells

57. 4. Interferons Three types 1.α interferons: -Produced by leukocytes to attract and stimulate NK cells 2.β interferons: -Produced by virus infected cells to trigger neighboring cells to produce antiviral proteins to slow viral replication 3.γ interferons: -Produced by T and NK cells to stimulate macrophage activity

58. 5. Complement 11 complement proteins + 9 other factors & regulators act in cascade to cause foreign cell lysis (often target bacteria) 1.Classical Pathway 2.Alternate Pathway

59. Figure 22–12 Complement Activation

60. 5. Complement The Classical Pathway Fast method Requires bound antibodies -C1 binds antibody on bacteria -Turns on C2 + C4 -C3 converts to C3b -C3b binds bacteria

61. 5. Complement The Alternative Pathway Slow method No antibodies required -Factors P (properdin), B, D interact in response to foreign material -C3 converted to C3b -C3b binds foreign material

62. 5. Complement Binding of C3b = “complement fixation” –Triggers anti-microbial effects 1.Trigger phagocytosis -Attract phagocytes and makes bacteria easier to grab and digest 2.Promotes inflammation -Causes release of histamine from basophils and mast cells 3.Catalyzes formation of MAC (membrane attack complex) -C5-C9 assemble to form pores on the membrane of the target cells resulting in cell lysis/death

63. 6. Inflammation Localized redness, swelling, heat, and pain in response to any tissue damage Function 1.Help prevent injury/infection from spreading 2.Disposes of cell debris 3.Sets the stage for repair

64. Figure 22–13 Inflammation and Tissue Repair

65. 6. Inflammation Events 1.Histamine is released by mast cells in response to change in the local environment  triggers an acceleration of blood flow to the area (vasodilation). 2.Clotting factors and complement enter the site. A clot forms around the injury and complement lyses bacteria and attracts phagocytes. 3.The local temperature rises due to the increase blood flow  accelerates enzymatic reactions to enhance killing of pathogens.

66. 6. Inflammation Events continued: 4.Neutrophils arrive (emigrate and chemotax)  activated to produce the respiratory burst releasing toxic compounds to kill pathogens. They also release cytokines to attract other phagocytes 5.Macrophages arrive to engulf pathogens and cell debris 6.Fibroblast are stimulated  create collagen patch (scar tissue) to reinforce the clot and begin repair 7.Mast cell chemicals trigger pain receptors 8.The specific/immune defenses are activated

67. Products of Inflammation 1.Puss: -Dead WBCs, pathogens, debris -Failure to clear  abscess (puss walled off by CT) 2.Necrosis: -Tissue degeneration due to lysosomal enzymes released by damaged cells -Injury gets worse before better 3.Apoptosis: -Controlled cell death (not necrosis)

68. 7. Fever Elevated body temperature –>99 ⁰F/37.2⁰C Triggered by pyrogens, material that causes the hypothalamus to raise body temperature: –Released into blood by leukocytes (mostly macrophages) when exposed to foreign antigens Effect –Increase metabolic rate to allow better defense and repair Rate increases 10%/1⁰C

69. 7. Fever Temperature up to 104 ⁰F: safe & productive At 106⁰F  nervous tissue dysfunctional At 110⁰F  proteins denature = death

70. A rise in the level of interferon in the body would suggest what kind of infection? A.chronic bacterial infection B.acute bacterial infection C.viral infection D.internal infection, as opposed to a dermal infection

71. What effects do pyrogens have in the body? A.release complement B.increase temperature/cause fever C.stimulate NK cells D.release interferon

72. Nonspecific and Specific Defenses Operate together to provide resistance to infection and disease

73. Specific resistance. The forms and properties of immunity.

74. Specific Defenses Protect against specific pathogens Depend on activities of lymphocytes Specific resistance (immunity): –develops after exposure to environmental hazards

75. Specific or Adaptive Defenses = The Immune Response T cells –Cellular immunity (cell-mediated immunity) –Function to amplify the inflammatory response B cells –Humoral immunity (antibody-mediated immunity) –Responsible for most complement activation/fixation B and T cells covered in receptors that recognize and bind only one specific antigen

76. Figure 22–15 (Navigator) The Immune Response

77. Antigen –Foreign substance that can activate the immune system and provoke an immune response –Usually large complex molecules Proteins, nucleic acids, some lipids, some polysaccharides Simple chemical structures like plastic and metal are not immunogic/antigenic

78. Figure 22–14 Forms of Immunity Vaccinations Antiserum Antiserum = Purified antibody solution against a particular antigen

79. 4 Properties of Immunity 1.Specificity 2.Versatility 3.Memory 4.Tolerance

80. Properties of Immunity 1.Specificity -Immune response targets particular antigens -Each B and T cell response to and destroys only one specific antigen 2.Versatility -A large diversity of lymphocytes prescribed by genes exist to respond to almost any antigen -When a particular antigen is encountered the one lymphocyte specific to it divides by clonal selection  produce many cells specific to that particular antigen

81. Properties of Immunity 3.Memory -Response after second exposure to the same antigen is faster, stronger, and last longer -During initial exposure memory cells were created to respond quickly upon second exposure 4.Tolerance -Immune system responds only to non-self antigens -B and T cells that recognize self antigens are destroyed by clonal deletion to insure self tolerance

82. T Cells and Cell Mediated Immunity Targets virus or parasite infected cells, cancer cells, and cells of foreign grafts 3 Main types of cells: 1.Cytotoxic T (T C ) cells: -Carry out cell mediated immunity -Physically attack foreign cells 2.Helper T (T H ) cells: -Activated B and T C cells 3.Suppressor T (T S ) cells: -Moderate the immune response by inhibiting T C and B cells

83. T cells must be activated by exposure to antigen Do not recognize free antigen Antigen must be bound to special glycoprotein receptors on target cell: Major Histocompatibility Complex (MHC) T Cells and Cell Mediated Immunity

84. MHC Proteins The membrane glycoproteins that bind to antigens Genetically coded in chromosome 6: –the major histocompatibility complex (MHC) –differs among individuals

85. Class I MHC - Found on all nucleated cells - Secreted by the Golgi - Bind endogenous antigens (small peptides present in the cytoplasm) - Abnormal peptides (cancer, virus, bacterial) trigger cell destruction by T C Cells Figure 22–16a (Navigator)

86. Class I MHC Proteins Pick up small peptides in cell and carry them to the surface: –T cells ignore normal peptides –abnormal peptides or viral proteins activate T cells to destroy cell

87. Figure 22–16b Antigen Presentation Class II MHC

88. Class II MHC Found on lymphocytes and Antigen Presenting Cells (APC) –APC = dendritic cells, Langerhans cells, macrophages, activated B cells –APC are responsible for activating T cells against foreign cells and proteins Bind exogenous antigens (material that have been phagocytosed and broken down) Activated T H cells which activate B cells and T C cells

89. Class I and Class II MHC Each T cell detects only one antigen and only when it is in either class I MHC or class II MHC Class recognized is determined by CD (cluster of differentiation) markers on the T cell (glycoprotein receptors) CD8  T C and T S –Respond to antigen in class I MHC CD4  T H –Respond to antigen in class II MHC

90. CD3 Receptor Complex –Found in all T cells CD8 Markers –Found on cytotoxic T cells and suppressor T cells –Respond to antigens on Class I MHC proteins CD4 Markers –Found on helper T cells –Respond to antigens on Class II MHC proteins CD8 or CD4 Markers –Bind to CD3 receptor complex –Prepare cell for activation

91. The mechanisms of T cell activation.

92. Figure 22–17 (Navigator) Activation of CD8/T C cells/Killer T

93. 1.Cell finds target antigen in class I MHC 2.T C cell undergoes clonal selection -Proliferation producing many identical cells, often requires stimulation from a T H cell that was activated by an APC) 3.Some clones remain inactive as memory T C cells 4.Some clones (active cells) destroy target cells 1.Release perforin: lyse target 2.Release lymphotoxin: disrupt DNA 3.Induce apoptosis: “self-destruct”

94. Activation of initial cell and clonal selection take time –Memory cells are ready to go upon second exposure to same antigen T S cells activation more slowly than T C function to release inhibitory cytokines to reduce immune response Activation of CD8/T C cells/Killer T

95. Organ Transplants Graft rejection: –Tissue typing = attempt to match MHC, but antigens in MHC will always be foreign, thus attacked –Need immuno-suppressive drugs to suppress T C cell activity to save graft

96. Activation of CD4 / Helper T Cells Figure 22–18

97. 1.Bind antigen in class II MHC 2.Proliferation / clonal selection 3.Memory cells 4.Active Helper T cells Activation of CD4 / Helper T Cells

98. Activated T H cells secrete cytokines which coordinate specific and nonspecific defense Activation of CD4 / Helper T Cells

99. 4 Functions of Cytokines 1.Stimulate T cell divisions: –produce memory T cells –accelerate cytotoxic T cell maturation 2.Attract and stimulate macrophages 3.Attract and stimulate NK cells 4.Promote activation of B cells resulting in antibody production

100. Memory T c Cells Produced with cytotoxic T cells Stay in circulation Immediately form cytotoxic T cells: –if same antigen appears again

101. Suppressor T Cells Secrete suppression factors Inhibit responses of T and B cells After initial immune response Limit immune reaction to single stimulus

102. Helper T Cells Activated CD4 T cells divide into: –active helper T cells: secrete cytokines –memory T cells: remain in reserve

103. Figure 22–19 Pathways of T Cell Activation

104. KEY CONCEPT Cell-mediated immunity involves close physical contact between activated T c cells and foreign, abnormal or infected cells T cell activation usually involves: –antigen presentation by phagocytic cell costimulation by cytokines from active phagocytes T c cells may destroy target cells through local release of cytokines, lymphotoxins, or perforin

105. The mechanisms of B cell activation.

106. B Cells and Antibody Mediated Immunity Targets bacteria, bacterial toxins, and free viruses

107. Figure 22–20 (Navigator) Activation of B cells: T dependent antigens

108. 1.B cells have antibodies (IgD) on surface as receptor for antigen -Binding causes B cell to become sensitized 2.Bound antigen is internalized, processed, and reappear back on the surface bound to Class II MHC protein 3.A specific T H cell recognizes the antigen+MHC complex and releases cytokines to activate the B cell 4.Activated B cell proliferates (clonal selection) to produce memory B cells and plasma cells Activation of B cells: T dependent antigens

109. 5.Plasma cells secrete antibodies specific to original antigen, ~2,000/sec, for 4-5 days, then die (apoptosis) 6.Memory B cells remain in reserve to respond to next infection Some B cells respond to T-independent antigens: - they can self activate upon antigen binding without a T H cell T-independent activation is less common and produces much weaker response and less protection Activation of B cells: T dependent antigens

110. Exposure to Antigen Initial exposure to antigen –~ 5 days B cell  plasma cell –~ 10 days to peak antibody levels (titer) in blood –Antibodies (IgM) circulate ~2 weeks Second exposure –Memory cell  plasma cell ~1-2 days –Peak titer ~2-3 days, higher level –Antibodies (IgG) circulate weeks - months

111. Figure 22–22 Primary and Secondary Responses Occur in both cell-mediated and antibody-mediated immunity

112. How can the presence of an abnormal peptide in the cytoplasm of a cell initiate an immune response? A.by stimulating production of pyrogens, beginning immune response B.by becoming attached to B cells which launch immune response C.by becoming attached to MHC and presented to T cells D.by altering the genetic programming of infected cell

113. A decrease in the number of cytotoxic T cells would affect which type of immunity? A.acquired immunity B.innate immunity C.humoral immunity D.cell-mediated immunity

114. How would a lack of helper T cells affect the antibody-mediated immune response? A.Response would not occur. B.Response would occur more quickly. C.Response would be lessened but present. D.Response would not be affected by loss of helper T cells.

115. A sample of lymph contains an elevated number of plasma cells. Would you expect the number of antibodies in the blood to be increasing or decreasing? A.increasing B.decreasing

116. Would the primary response or the secondary response be more affected by the lack of memory B cells for a particular antigen? A.primary response B.secondary response

117. The structure of an antibody, and the types of antibodies found in body.

118. Figure 22–21a, b Antibody Structure Humans produce 100 million – 1 billion different antibodies that each bind a different antigen

119. Antibody (Ab) Structure 2 parallel pairs of polypeptide chains: –1 pair of identical heavy chains –1 pair of identical light chains Held together by disulfide bonds Hinge region = flexibility Each chain contains: –constant segments (C) Determine class of antibody molecules Have sites for complement binding (Fc region) –variable segments (V) Determine antigen specificity of antibody Make up antigen bind sites

120. 5 Heavy-Chain Constant Segments Determine 5 types of antibodies: –IgG –IgE –IgD –IgM –IgA

121. Classes of Antibodies/Immunoglobulins 1.IgG antibodies -Monomer -Most common -Produce upon second exposure -Produced at high levels -Provides resistance against viruses, bacteria, and toxins -Can cross placenta 2.IgM antibodies -Pentamer (5) -First class produced upon initial exposure -Forms immune complexes (agglutination)

122. Classes of Antibodies/Immunoglobulins 3.IgA antibodies -Dimer -In secretions 4.IgD antibodies -Monomer -On surface of B cells as receptor -Sensitizes or activates B cell upon antigen binding 5.IgE antibodies -Monomer -On Mast cells and basophils as receptor -Triggers histamine release upon antigen binding

123. Figure 22–21c, d Antibody Function

124. Antigen–Antibody Complex Antibodies bind antigen via antigen binding sites Antigen gets bound by its antigenic determinant site (epitope) –Epitope = the part of an antigen that is recognized by the immune system, specifically by antibodies, B cells, or T cells. Complete antigen = two epitopes bound to one site –can lead to allergies when they combine with body proteins (e.g. latex)

125. 7 Functions of Antigen–Antibody Complexes 1.Neutralization of antigen binding sites 1.Prevent attachment or pathogens 2.Inactivate toxins 2.Precipitation and agglutination: –formation of immune complex 3.Activation of complement/complement fixation 4.Attraction of phagocytes

126. 7 Functions of Antigen–Antibody Complexes 5. Opsonization: –increasing phagocyte efficiency 6.Stimulation of inflammation -IgE on Mast cell 7.Ab-dependent cell mediated cytotoxicity -Prevention of bacterial and viral adhesion

128. Table 22–1 5 Classes of Antibodies

129. KEY CONCEPT Antibody-mediated immunity involves the production of specific antibodies by plasma cells derived from activated B cells B cell activation usually involves: –antigen recognition, through binding to surface antibodies –costimulation by a T H cell Antibodies produced by active plasma cells bind to target antigen and: –inhibit its activity –destroy it –remove it from solution –promote its phagocytosis by other defense cells

130. Immune Disorders 1.Autoimmune Disorders -Immune response targets normal body cells, auto-antibodies produced -Insulin dependent diabetes mellitus/Type I -Attacks cells of pancreas -Multiple sclerosis -Attack white matter of CNS -Rheumatoid arthritis -Attack joints -Graves Disease -Stimulate thyroid

131. 2.Immunodeficiency Diseases -Immune system fails to develop or immune responses are blocked -Cause: -Genetics/development, infection by virus, exposure to radiation/drugs -SCID (severe combined immuno-deficiency disorder) -“Bubble Boy”, born without B or T cells -Hodgkins Disease -Lymph node cancer = decrease B and T cells Immune Disorders

132. AIDS Acquired immune deficiency syndrome Virus (HIV) infects CD4 (T H ) cells and replicates causing cell lysis –T H cells necessary for both T C and B cell activation –Decreased T H  patient has poor cell mediated and antibody mediated immunity –Patient dies of opportunistic infections

133. Allergies Excessive immune response to non-harmful antigens, results in tissue damage 1.Immediate Hypersensitivity (most common) 1.Anaphylaxis: -Initial exposure produces IgE -IgE bind mast cells/basophils -2 nd exposure, allergen binds IgE, triggers release of histamine and heparin  inflammation -Example, runny eyes and nose -Anaphylatic shock = allergen circulates in blood  body wide inflammation (decrease BP = shock) 2.Atopy - full blown allergic response upon 1 st exposure

134. Allergies 2.Delayed Hypersensitivity -Cell mediated -T C, T H, and macrophages activated by allergen resulting in cell death and local inflammation -Example, poison ivy

135. Age Related Changes Thymus size decreases  less T cells produced Decrease T H cells  less B and T C cell activation  decrease immunity overall Decrease B cells  decrease antibodies  increase susceptibility to viral and bacterial infections Increase chance of cancer –Decrease NK and T C cells

136. Figure 22–23 Summary of the Body Defense Specific and nonspecific defenses are linked

137. Figure 22–24 Body Responses to Bacterial Infection

138. Table 22–2 Summary: Cells of the Immune System

139. SUMMARY Divisions of the lymphatic system: –lymphatic vessels (lymphatics), lymph, lymphoid tissues and organs Types of lymphocytes: –T cells, B cells, NK cells Lymphoid tissues and organs: –Nodules, nodes, MALT, thymus, spleen

140. SUMMARY 7 nonspecific defenses: –physical barriers –phagocytes –immunological surveillance –interferons –complement –inflammation –Fever Specific defenses: –cell-mediated immunity –antibody mediated immunity

141. SUMMARY Forms of immunity: –innate or acquired –active or passive Properties of immunity: –specificity, versatility, memory, and tolerance T cells and cell-mediated immunity: –antigen presentation –MHCs and APCs –antigen recognition –CD8 T cell activation –CD4 T cell activation

142. SUMMARY B cells and antibody-mediated immunity: –sensitization –plasma cells and memory B cells –antibody structure –antigen–antibody complex –5 classes of immunoglobins Immune disorders Effects of aging on the immune response