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BMS 251 Ch. 22

by: Claire Neville

BMS 251 Ch. 22 BMS 251-20

Claire Neville
GPA 3.209
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About this Document

Immune System Notes
Anatomy & Physiology II
Dr. Tara Alger
Class Notes
BMS 251, Biomedical Science, anatomy, Physiology, immune system, T-cells, B-cells, White Blood Cells




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This 13 page Class Notes was uploaded by Claire Neville on Thursday February 25, 2016. The Class Notes belongs to BMS 251-20 at Grand Valley State University taught by Dr. Tara Alger in Winter 2016. Since its upload, it has received 33 views. For similar materials see Anatomy & Physiology II in Biomedical Sciences at Grand Valley State University.

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Date Created: 02/25/16
Chapter  22  Immune  System   Immune  System   •   Protects  us  from  infectious  agents  and  harmful  substances   o   Typically  without  our  awareness   •   Composed  of  numerous  cellular  and  molecular  structures   •   Function  dependent  on  specific  type  of  infectious  agent     22.1  Overview  of  Diseases-­‐  Caused  by  Infectious  Agents   •   Infectious  agents  can  damage  or  kill  a  host   o   Pathogenic  agents  are  ones  that  cause  harm   o   Five  major  categories:     §   Bacteria   §   Viruses   §   Fungi   §   Protozoans   §   multicellular  parasites   •   Bacteria:  single-­‐celled  prokaryotes   o   Small  (1    to  2  µm)  cell  with  both  a  membrane  and  a  cell  wall   o   Varied  types:  spherical  (cocci),  rodlike  (bacilli),  or  coiled  (spirilla)   o   Most  bacteria  harmless;  some  virulent  (cause  serious  illness)   §   Examples  of  virulent  bacteria:  Clostridium  tetani  (tetanus),  streptococcal  bacteria  (strep   throat)   •   Viruses:  pieces  of  DNA  or  RNA  in  a  protein  shell   o   Viruses  are  not  cells—they  are  much  smaller     §   Only  about  one-­‐hundredth  of  a  micrometer     o   Obligate  intracellular  parasites   §   Virus  must  enter  a  cell  to  reproduce   §   Direct  infected  cell  to  make  copies  of  nucleic  acid  and  capsid  (shell)   §   The  virus  or  immune  response  may  kill  the  host  cell   o   E.g.,  common  cold,  ebola,  chickenpox   •   Fungi:  eukaryotic  cells  with  membrane  and  cell  wall   o   Include  molds,  yeasts,  multicellular  fungi  that  produce  spores   o   Release  proteolytic  enzymes  inducing  inflammation   o   Cause  superficial  diseases  in  the  integument  (e.g.,  athletes  foot)     o   Can  infect  mucosal  linings  (e.g.,  vaginal  yeast  infections)  or  cause  internal  infections  (e.g.,   histoplasmosis)   •   Protozoans:  eukaryotic  cells  without  a  cell  wall   o   Intracellular  and  extracellular  parasites   o   Disease  examples:  malaria  and  trichomoniasis   •   Multicelluar  parasite  are  nonmicroscopic   o   Take  nourishment  from  host  they  live  in   o   E.g.,  tapeworm   •   Prions:  fragments  of  infectious  proteins   o   Neither  cells  nor  viruses   o   Cause  disease  in  nervous  tissue   o   E.g.,  Variant  Creutzfeldt-­‐Jakob  disease  (“mad  cow”)-­‐  in  humans   §   Can  be  spread  from  cows  to  human  by  consuming  infected  meat   •   Cancer   o   Immune  system  is  on  alert  for  cancer  cells   o   Still  an  infection  agent!     22.2a  Immune  Cells  and  Their  Locations   •   Leukocytes  (WBC)   o   Formed  in  red  bone  marrow   o   Granulocytes:  neutrophils,  eosinophils,  basophils   o   Monocytes     §   Become  macrophages  when  they  leave  blood  and  enter  tissues   o   Lymphocytes   §   B-­‐lymphocytes,  T-­‐lymphocytes,  NK  (natural  killer)  cells   •   Structures  that  house  immune  system  cells   o   Most  leukocytes  are  in  body  tissues  (instead  of  blood)     o   Lymphatic  tissue-­‐  secondary  structures   §   T-­‐  and  B-­‐lymphocytes,  macrophages,  dendritic  cells,  and  NK  cells  housed  in  lymph  nodes,   spleen,  tonsils,  MALT,  lymphatic  nodules   o   Select  organs  house  macrophages   §   May  be  permanent  residents  of  the  organ,  or  migrating  macrophages   •   Structures  that  house  immune  system  cells  (continued)   o   Dendritic  cells   §   Located  in  Epithelial  layers  of  skin  and  mucosal  membranes   §   These  dendritic  cells  are  usually  derived  from  monocytes   §   Engulf  pathogens  and  migrate  into  lymph   o   Mast  cell   §   Located  in  connective  tissue   §   Mast  cells  typically  in  close  proximity  to  small  blood  vessels   §   Abundant  in  dermis  and  mucosa  of  respiratory,  GI,  and  urogenital  tracts   §   Also  found  in  connective  tissue  of  organs  (e.g.,  endomysium  of  muscle)   22.2b  Cytokines   •   Cytokines:  small  proteins  that  regulate  immune  activity   o   Produced  by  cells  of  both  innate  and  adaptive  immune  system   o   Chemical  messengers  released  from  one  cell  that  bind  to  receptors  of  target  cells     o   Effects   §   Signaling  cells     §   Controlling  development  and  behavior  of  immune  cells   §   Regulating  inflammatory  response   §   Destroying  cells   •   Cytokine  examples   o   Interferons:  targeting  pathogens  and  triggering  the  immune  defense   §   E.g.,  IFN-­‐α   o   Colony-­‐stimulating  factor  (CSF):  development  and  differentiation  of  all  blood  cells   §   E.g.,  granulocyte  CSF,  GM-­‐CSF   22.2c  Comparison  of  Innate  Immunity  and  Adaptive  Immunity   •   Two  types  of  immunity  differ  based  on   o   Cells  involved   o   Specificity  of  cell  response   o   Mechanisms  of  eliminating  harmful  substances   o   Amount  of  time  for  response   •   Although  innate  and  adaptive  immunities  are  distinct,  they  work  together  in  body  defense   •   Innate  immunity:  present  at  birth   o   Protects  against  variety  of  different  substances  (nonspecific)   §   No  prior  exposure  to  substance  necessary   o   Includes  barriers  of  skin  and  mucosal  membranes,  nonspecific  cellular  and  molecular  internal   defenses   o   Respond  immediately  to  potentially  harmful  agents   •   _Adaptive  immunity_:  acquired  immunity   o   Response  to  antigen  involves  specific  T-­‐  and  B-­‐lymphocytes   §   These  cells  are  then  specific  for  what  they  will  target  (only  certain  antigens)   o   Takes  several  days  to  be  effective     22.3  Innate  Immunity   •   Characteristics  of  innate  immunity   o   Prevents  entry  of  potentially  harmful  substances   o   Responds  nonspecifically  to  a  range  of  harmful  substances   o   First  line  of  defense  is  skin  and  mucosal  membrane   o   Second  line  of  defense  involves  internal  processes   §   Cells:   •   neutrophils,  macrophages,  dendritic  cells,  eosinophils,  basophils,  and  NK  cells   §   Chemicals:   •   interferon  and  complement   §   Processes:   •   inflammation  and  fever   22.3a  Preventing  Entry   •   Few  microbes  can  penetrate  intact  skin   o   Physical  barrier  of  epidermis  and  dermis   o   Skin  releases  antimicrobial  substances   §   lysozyme,  sebum,     o   Has  normal  nonpathogenic  flora  (microorganisms)   §   Help  prevent  growth  of  pathogenic  microorganisms   •   Mucosal  membranes  line  body  openings   o   Produce  mucin  and  release  antimicrobial  substances   §   Defensins,  lysozyme,  IgA   o   Lined  by  harmless  bacteria  that  suppress  growth  of  more  virulent  types   22.3b  Cellular  Defenses   •   Neutrophils,  macrophages,  and  dendritic  cells   o   Cells  of  innate  immunity  that  engulf  unwanted  substances  by  phagocytosis   o   Neutrophils  and  _macrophages_  destroy  engulfed  particles   §   Intake  vesicle  fuses  with  lysosome  forming  phagolysosome   §   Digestive  enzymes  break  down  the  unwanted  substances   §   Degraded  residue  is  released  by  exocytosis   o   _dendritic  cells_  destroy  particles  and  then  present  fragments   §   Antigens  are  presented  on  dendritic  cell  surface  to  T-­‐lymphocytes   •   Necessary  for  initiating  adaptive  immunity   •   Basophils  and  mast  cells  promote  inflammation   o   Basophils  circulate  in  the  blood   o   Mast  cells  reside  in  connective  tissue,  mucosa,  internal  organs   o   They  release  granules  containing  chemicals   §   The  chemicals  increase  movement  of  fluid  from  blood  to  injured  tissue   §   They  attract  immune  cells  (are  chemotactic)   §   Histamine  increases  vasodilation  and  capillary  permeability   §   Heparin  acts  as  an  anticoagulant   o   Eicosanoids  released  from  their  plasma  membrane  also  increase  inflammation   •   Natural  Killer  cells  destroy  a  variety  of  unwanted  cells   o   “NK  cells”  form  in  bone  marrow,  circulate  in  blood,  and  accumulate  in  secondary  lymphatic   structures   §   Perform  immune  surveillance—patrol  the  body  detecting  unhealthy  cells   o   They  destroy  virus-­‐infected  cells,  bacteria-­‐infected  cells,  tumor  cells,  cells  of  transplanted  tissue   o   They  kill  by  releasing  cytotoxic  chemicals   §   Perforin  creates  a  transmembrane  pore  in  unwanted  cell   §   Granzymes  enter  pore  and  cause  apoptosis  (death)  of  cell   •   Eosinophils  attack  multicellular  parasites   o   Degranulate,  release  enzymes  and  other  toxic  substances     §   Can  release  proteins  that  form  transmembrane  pores  in  parasite’s  cells   o   Participate  in  immune  responses  of  allergy  and  asthma   o   Engage  in  phagocytosis  of  antigen-­‐antibody  complexes   •   22.3c  Antimicrobial  Proteins   •   Antimicrobial  proteins  are  molecules  that  function  against  microbes   •   Interferons:  a  class  of  cytokines  that  nonspecifically  impede  viral  spread   o   IFN-­‐a  and  IFN-­‐b    produced  by  leukocytes  and  virus-­‐infected  cells   §   Bind  to  neighboring  cells  and  prevent  their  infection   §   Stimulate  NK  cells  to  destroy  virus-­‐infected  cells   •   Complenment  system:  group  of  over  30  plasma  proteins   o   Work  along  with  (“complement”)  antibodies   o   Identified  with  letter  “C”  and  number  (e.g.,  C2)   o   Synthesized  by  liver,  continuously  released  in  inactive  form   o   Complement  activation  follows  pathogen  entry     o   Especially  potent  system  against  bacterial  infections   o   4  modes  of  action     §   Opsonization   §   Inflammation   §   Cytolysis   §   Elimination  of  immune  complexes   o   Opsonization:  complement  protein  (opsonin)  binds  to  pathogen   §   Enhances  likelihood  of  phagocytosis  of  pathogenic  cell   o   Inflammation:  is  enhanced  by  complement   §   Activates  mast  cells  and  basophils   §   Attracts  neutrophils  and  macrophages   §   Diapedsis  and  chemotaxis   o   Cytolysis:  complement  triggers  splitting  of  target  cell   §   Complement  proteins  form  membrane  attack  complex  (MAC)  that  creates  channel  in   target  cell’s  membrane   •   Fluid  enters,  causing  cell  lysis   o   Elimination  of  immune  complexes   §   Complement  links  antigen-­‐antibody  complexes  to  erythrocytes   §   Cells  move  to  liver  and  spleen  where  complexes  are  stripped  off   22.3d  Inflammation   •   Inflammation:  an  immediate  response  to  ward  off  unwanted  substances   o   Local,  nonspecific  response  of  vascularized  tissue  to  injury   o   Part  of  innate  immunity   •   Events  of  inflammation   o   Injured  tissue,  basophils,  mast  cells,  and  infectious  organisms  (bacteria)  release  chemicals  that   initiate  response   §   The  chemicals  include  histamine,  and  chemotactic  (chemical  lure)  factors   o   Released  chemicals  cause  vascular  changes   §   Vasodilation   §   Increased  capillary  permeability   §   Increased  endothelial  expression  of  molecules  for  leukocyte  adhesion   •   Cell-­‐adhesion  molecules,  CAMs   o   Recruitment  of  leukocytes   §   Margination  adherence  of  leukocytes  to  endothelial  CAMs   §   Diapedesis:  cells  escape  blood  vessel  walls   §   Chemotaxis:  leukocytes  migrate  toward  chemicals  released  from  damaged,  dead,  or   pathogenic  cells   •   Leukocytes  release  cytokines  stimulating  leukopoiesis  in  marrow   •   Macrophages  may  release  pyrogens  (fever-­‐inducing  molecules)   o   Delivery  of  plasma  proteins  to  site   §   Immunoglobulins,  complement,  clotting  proteins,  and  kinins   §   Clotting  proteins  form  clots  that  wall  off  microbes   •   Effects  of  inflammation   o   Fluid  moves  from  blood  to  injured  or  infected  area     §   Liquid  contains  fluid,  protein,  and  immune  cells  to  eliminate  pathogens  and  promote   healing   §   Vasodilation  brings  more  blood  to  the  area   §   Loss  of  plasma  proteins  decreases  capillary  osmotic  pressure,  thus  decreasing  fluid   reabsorption  into  blood   §   Extra  fluid  is  taken  up  by  lymphatic  capillaries  in  the  area  (“washing”)   •   Carries  away  debris  and  allows  lymph  node  monitoring  of  its  contents     o   Within  72  hours,  inflammatory  response  slows   §   Monocytes  exit  blood  becoming  macrophages     §   Macrophages  eat  bacteria,  damaged  host  cells,  dying  neutrophils     §   Tissue  repair  begins  as  fibroblasts  form  new  connective  tissue   •   Cardinal  signs  of  inflammation   o   Redness  from  increased  blood  flow   o   Heat  from  increased  blood  flow  and  increased  metabolic  activity  within  the  area   o   Swelling  from  increase  in  fluid  loss  from  capillaries   o   Pain  from  stimulation  of  pain  receptors     o   Loss  of  function  from  pain  and  swelling  in  severe  cases   •   Duration  of  acute  inflammation:  about  8  to  10  days   22.3e  Fever   •   Fever  (pyrexia):  abnormal  body  temperature  elevation   o   1°C    or  more  from  normal  (37°C)   o   Results  from  the  release  of  pyrogens  (e.g.,  IL-­‐1)  from  immune  cells  or  infectious  agents   •   Events  of  fever   o   Pyrogens  circulate  through  blood  and  target  hypothalamus   o   Hypothalamus  raises  temperature  set  point  leading  to  fever   o   Fever  stages:  onset,  stadium,  and  defervescence   o   Onset:    temperature  begins  to  rise   §   Hypothalamus  stimulates  dermis  blood  vessels  to  constrict  (less  heat  loss)   §   Shivering  of  muscle  generates  more  heat  (may  be  in  response  to  chills)   o   Stadium:    elevated  temperature  is  maintained   §   Metabolic  rate  increases  to  promote  elimination  of  harmful  substance   §   Liver  and  spleen  bind  zinc  and  iron  thereby  slowing  microbial  reproduction   o   Defervescence:    time  when  temperature  returns  to  normal   §   Hypothalamus  no  longer  stimulated  by  pyrogens   §   Hypothalamus  stimulates  mechanisms  to  release  heat     •   E.g.,  vasodilation  of  skin  blood  vessels,  sweating   •   Benefits  of  fever   o   Inhibits  reproduction  of  bacteria  and  viruses   o   Promotes  interferon  activity   o   Increases  activity  of  adaptive  immunity   o   Accelerates  tissue  repair   o   Increases  CAMs  on  endothelium  of  capillaries  in  lymph  nodes   o   Recommended  to  leave  a  low  fever  untreated   •   Risks  of  a  high  fever   o   High  fevers  potentially  dangerous   §   103ºF  in  children,  slightly  lower  in  adult   o   Changes  in  metabolic  pathways  and  denaturation  of  proteins  pose  risks   o   Possible  seizures   o   Irreversible  brain  damage  at  greater  than  106ºF   o   Death  likely  if  temperature  greater  than  109ºF     22.4  Adaptive  Immunity:  An  Introduction   •   Adaptive  immunity  involves  specific  lymphocyte  responses  to  an  antigen   o   Contact  with  antigen  causes  lymphocyte  proliferation   o   Immune  response    consists  of  lymphocytes  and  their  products   o   Longer  response  time  than  innate  immunity   §   Since  it  takes  days  to  develop,  adaptive  immunity  is  considered  the  third  line  of  body’s   defense   •   Two  branches  of  adaptive  immunity   o   Cell-­‐mediated  immunity  involving  T-­‐lymphocytes   o   Humoral  immunity  involving  B-­‐lymphocytes,  plasma  cells,  and  antibodies   22.4a  Antigens   •   Pathogens  are  detected  by  lymphocytes  because  they  contain  antigens   •   Antigen:    substance  that  binds  a  T-­‐lymphocyte  or  antibody   o   Antigen  is  usually  a  protein  or  large  polysaccharide   o   Examples  of  antigens   §   Protein  capsid  of  viruses   §   Cell  wall  of  bacteria  or  fungi   §   Bacterial  toxins   §   Abnormal  proteins  or  tumor  antigens   •   Foreign  antigens  versus  self-­‐antigens   o   Foreign  antigen    differ  from  human  body’s  molecules   §   Bind  body’s  immune  components   o   Self-­‐antigen      are  body’s  own  molecules   §   Typically  do  not  bind  immune  components   o   Immune  system  generally  able  to  distinguish   §   However  in  autoimmune  disorders    the  system  reacts  to  self-­‐antigens  as  if  foreign   •   Antigenic  determinant     o   Specific  site  on  antigen  recognized  by  immune  system   o   Each  has  a  different  shape   o   Pathogenic  organisms  can  have  multiple  determinants   •   Immunogen:    antigen  that  induces  an  immune  response   •   Immunogenicity:  ability  to  trigger  response   §   Increases  with  antigen’s  degree  of  foreignness,  size,  complexity,  or  quantity   •   Haptens:    small  foreign  molecules  that  induce  immune  response  when  attached  to  a  carrier  molecule   in  host   o   E.g.,  toxin  in  poison  ivy   o   Account  for  hypersensitivity  reactions     §   E.g.,  to  drugs  such  as  penicillin,  pollen   22.4b  General  Structure  of  Lymphocytes   •   T-­‐  and  B-­‐lymphocytes  have  unique  Receptor  complexes   o   About  100,000  per  cell   o   Each  complex  binds  one  specific  antigen   o   TCR    (T-­‐cell  receptor)  is  antigen  receptor  of  T-­‐lymphocyte     o   BCR    (B-­‐cell  receptor)  is  antigen  receptor  of  B-­‐lymphocyte     22.4b  General  Structure  of  Lymphocytes   •   Lymphocyte  contact  with  antigen   o   B-­‐lymphocytes  make  direct  contact  with  antigen   o   T-­‐lymphocytes  have  antigen  presented  by  some  other  cell   §   Antigen  is  processed  and  presented  by  another  cell  type   §   T-­‐lymphocyte  coreceptors  (e.g.,  CD  proteins)  facilitate  the  interaction   •   T-­‐lymphocyte  subtypes   o   Helper  T-­‐Lymphocytes  are  CD4+  cells   §   Assist  in  cell-­‐mediated,  humoral,  and  innate  immunity   •   E.g.,  activate  NK  cells  and  macrophages   o   Cytotoxic  T-­‐lymphocytes    are  CD8+  cells   §   Release  chemicals  that  destroy  other  cells   o   Other  types  include  memory  T-­‐cells   22.4c  Antigen-­‐Presenting  Cells  and  MHC  Molecules   •   Antigen  Presentation:    cells  display  antigen  on  plasma  membrane     o   so  T-­‐cells  can  recognize  it   o   Two  categories  of  cells  present  antigens   §   All  nucleated  cells  of  the  body   §   Antigen  Presenting  Cells  (APCs)   •   Immune  cells  that  present  to  both  helper  T-­‐cells  and  cytotoxic  T-­‐cells   •   Include:  dendritic  cells,  macrophages,  B-­‐lymphocytes   o   Requires  attachment  of  antigen  to  Major  Histocompatibility  complex  (MHC)       §   MHC  is  group  of  transmembrane  proteins   §   MHC  I  is  found  on  all  nucleated  cells   §   MHC  I  &  II  is  found  on  APCs   •   Synthesis  and  display  of  MHC  class  I  molecules  on  nucleated  cells   o   MHC  class  I  molecules   §   Have  genetically  determined  structure  that  is  unique  to  individual   §   Display  fragments  of  proteins  on  the  surface  of  the  cell   •   If  fragments  are  from  endogenous  proteins,  immune  system  recognizes  them  as   “self ”  and  ignores  them   •   If  fragments  are  from  an  infectious  agent,  immune  system  considers  the  antigen   “nonself ”   o   Communicates  to  cytotoxic  T-­‐cells  that  they  should  destroy  cell   •   Display  of  MHC  class  II  molecules  on  professional  antigen-­‐presenting  cells   o   MHC  class  II  molecules   §   Exogenous  antigens  brought  into  cell  through  endocytosis   §   Phagosome  merges  with  lysosome,  forming  phagolysosome   §   Substance  digested  into  peptide  fragments   §   Fragments  “loaded”  onto  MHC  class  II  molecules  within  vesicle   §   Vesicle  merges  with  plasma  membrane  with  antigen  bound  to  MHC  molecule   •   Provides  means  of  communicating  with  helper  T-­‐lymphocytes   22.4d  Overview  of  Life  Events  of  Lymphocytes   •   Three  main  events  in  life  of  lymphocyte   o   Formation  and  maturation  of  lymphocytes   §   Occurs  in  primary  lymphatic  structures  (red  marrow  and  thymus)   §   Become  able  to  recognize  one  specific  foreign  antigen   o   Activation  of  lymphocytes   §   In  secondary  lymphatic  structures  they  are  exposed  to  antigen  and  become  activated   §   Replicate  to  form  identical  lymphocytes   o   Effector  response:  action  of  lymphocytes  to  eliminate  antigen   §   T-­‐lymphocytes  migrate  to  site  of  infection   §   B-­‐lymphocytes  stay  in  secondary  lymphatic  structure  (as  plasma  cells)   •   Synthesize  and  release  large  quantities  of  antibodies     •   Antibodies  are  transported  to  infection  site  through  blood  and  lymph       22.5  Formation  and  Selection  of  Lymphocytes   •   Lymphocytes  are  formed  in  red  marrow   •   They  are  then  tested  for  immunocompetence     o   Immunocompetent  cells  bind  and  respond  to  antigen   o   Testing  occurs  during  development  and  shortly  after  birth   §   Occurs  in  primary  lymphatic  structures   22.5a  Formation  of  T-­‐lymphocytes   •   T-­‐lymphocytes  originate  in  red  bone  marrow   o   Migrate  to  thymus  as  pre-­‐T-­‐lymphocytes  to  complete  maturation   o   Initially  have  both  CD4  and  CD8  proteins   o   Possess  unique,  randomly  produced  TCR  receptor   o   Each  cell  has  its  TCR  “tested”  through  a  process  of  selection   §   Whether  it  can  bind  MHC  with  antigen   §   Whether  it  binds  only  foreign  (“nonself ”)  antigen   22.5b  Selection  of  T-­‐lymphocytes   •   Thymic  selection    eliminates  98%  of  T-­‐cells  produced   •   Positive  selection   o   Selects  for  the  ability  of  T-­‐cells  to  bind  thymic  epithelial  cells  with  MHC  molecules  (those  that   can  bind  survive)   •   Negative  selection     o   Tests  ability  of  T-­‐lymphocyte  to  NOT  bind  self-­‐antigens  (self-­‐tolerance)   o   Thymic  dendritic  cells  present  self-­‐antigens  and  T-­‐cells  that  bind  to  them  are  destroyed   22.5c  Differentiation  and  Migration  of  T-­‐Lymphocytes   •   T-­‐lymphocytes  differentiate   o   Helper  T-­‐lymphocytes  lose  CD8  protein   o   Cytotoxic  T-­‐lymphocytes  lose  CD4  protein   •   T-­‐lymphocytes  migrate  from  thymus  to  secondary  lymphatic  structures   o   They  are  immunocompetent   o   Naïve  T-­‐lymphocyte  not  yet  exposed  to  antigens  they  recognize     22.6  Activation  and  Clonal  Selection  of  Lymphocytes   •   Clonal  Selection:    forming  clones  in  response  to  an  antigen   o   All  formed  cells  have  same  TCR  or  BCR  that  matches  specific  antigen   •   Antigen  Selection:    first  encounter  between  antigen  and  lymphocyte   o   Usually  occurs  in  secondary  lymphatic  structures   §   Antigen  in  blood  taken  to  spleen   §   Antigen  penetrating  skin  transported  to  lymph  node   §   Antigen  from  respiratory,  GI,  urogenital  tracts,  in  tonsils  or  MALT   22.6a  Activation  of  T-­‐Lymphocytes   •   Activation  of  helper  T-­‐lymphocytes   o   First  Signal:    direct  contact  with  MHC  molecule  of  APC   §   APC  presents  exogenous  antigen  with  MHC  class  II  molecules   §   Occurs  in  secondary  lymphatic  structure   §   Specific  TCR  site  of  T-­‐cell  binds  to  antigen  peptide  fragment     •   Interaction  stabilized  by  CD4  molecule  of  helper  T-­‐lymphocyte   §   If  it  doesn’t  recognize  antigen,  T-­‐cell  disengages  quickly   §   If  it  does  recognize  antigen,  contact  lasts  several  hours   •   Activation  of  helper  T-­‐lymphocytes  (continued)   o   Second  Signal   §   Other  receptors  of  APC  and  T-­‐cell  interact   §   Helper  T-­‐cell  secretes  interleukin-­‐2,  stimulating  itself   §   Helper  T-­‐cells  proliferate  forming  clones  of  helpers  T-­‐cells  (with  same  TCR)   •   Some  cells  become  activated  helper  T-­‐lymphocytes  that  continue  to  produce  IL-­‐2   •   Some  cells  become  memory  helper  T-­‐lymphocytes,  available  for  future   encounters   22.6b  Activation  of  B-­‐Lymphocytes   •   B-­‐lymphocytes  need  to  be  activated,  but  can  respond  to  antigens  outside  of  cells   o   First  signal   §   Intact  antigen  binds  to  BCR,  cross-­‐linking  2  BCRs   §   Stimulated  B-­‐cell  engulfs,  processes,  and  presents  antigen  to  helper  T-­‐cell  for   recognition   o   Second  signal   §   Activated  helper  T-­‐cell  releases  IL-­‐4,  stimulating  B-­‐lymphocyte   •   B-­‐lymphocyte  activation   o   Causes  B-­‐lymphocytes  to  proliferate  and  differentiate   o   Most  differentiate  into  Plasma  Cells  that  produce  antibodies   o   Remainder  become  memory  B-­‐lymphocytes   §   Retain  BCRs  and  activate  with  reexposure  to  same  antigen   §   Have  much  longer  life  span  than  plasma  cells   o   In  some  cases  activation  occurs  without  T-­‐cells   §   But  production  of  memory  B-­‐cells  and  various  antibodies  requires  helper  T-­‐cell   involvement  in  activation   22.6c  Lymphocyte  Recirculation   •   Lymphocyte  recirculation   o   After  several  days,  a  lymphocyte  exits  secondary  lymphatic  structure   §   Circulates  through  blood  and  lymph   §   Different  lymphocytes  delivered  to  secondary  lymphatic  structures   §   Makes  it  more  likely  lymphocyte  will  encounter  specific  antigen     22.7  Effector  Response  at  Infection  Site   •   Effector  Response   o   Mechanism  used  by  lymphocytes  to  help  eliminate  antigen     o   Each  lymphocyte  type  has  its  own   §   Helper  T-­‐lymphocytes   •   Release  IL-­‐2  and  other  cytokines   •   Regulate  cells  of  adaptive  and  innate  immunity   §   Cytotoxic  T-­‐lymphocytes   •   Destroy  unhealthy  cells  by  apoptosis   §   Plasma  cells  (B-­‐lymphocytes)   •   Produce  antibodies   22.7a  Effector  Response  of  T-­‐Lymphocytes   •   Effector  response  of  helper  T-­‐lymphocytes   o   After  exposure  to  antigen  (in  secondary  lymphatic  structures),  activated  and  memory  helper  T-­‐ cells  migrate  to  infection  site   §   Continually  release  cytokines  to  regulate  other  immune  cells   o   Help  activate  B-­‐lymphocytes   o   Activate  cytotoxic  T-­‐lymphocytes  with  cytokines   o   Stimulate  activity  of  innate  immune  system  cells   •   Effector  response  of  cytotoxic  T-­‐lymphocytes   o   After  exposure  to  antigen,  activated  and  memory  cytotoxic  T-­‐cells  migrate  to  infection  site   o   They  destroy  infected  cells  that  display  the  antigen   §   Make  physical  contact  with  unhealthy  or  foreign  cell   §   After  recognizing  antigen,  cytotoxic  T-­‐cell  releases  granules  containing  perforin  and   granzymes  (cytotoxic  chemicals)   §   Perforin  forms  channel  in  target  cell  membrane   §   Granzymes  enter  channel  and  induce  death  by  apoptosis   o   Because  this  works  against  antigens  associated  with  cells,  the  system  is  called  cell-­‐mediated   immunity   22.7b  Effector  Response  of  B-­‐Lymphocytes   •   Most  activated  B-­‐lymphocytes  become  plasma  cells   •   Plasma  cells  synthesize  and  release  antibodies   o   The  cells  remain  in  the  lymph  nodes   o   Antibodies  circulate  through  lymph  and  blood  until  encountering  antigen   22.8a  Structure  of  Immunoglobulins   •   Antibodies:    immunoglobulin  proteins  produced  against  a     o   particular  antigen   o   Antibodies  “tag”  pathogens  for  destruction  by  immune  cells   o   Good  defense  against  viruses,  bacteria,  toxins,  yeast  spores   •   Structure:  Y-­‐shaped,  soluble  proteins   o   Composed  of  four  polypeptide  chains   §   Two  identical  heavy  chains  and  two  identical  light  chains   §   Held  together  by  disulfide  bonds  to  form  antibody  monomer   §   Two  important  functional  areas,  variable  and  constant  regions   •   Variable  regions   o   Located  at  the  ends  of  the  antibody  “arms”   §   Contain  antigen-­‐binding  site  (most  antibodies  have  two  sites)   •   Constant  Region   o   Contains  the  Fc  region,  which  determines  biological  function   22.8b  Actions  of  Antibodies   •   Neutralization   o   Antibody  physically  covers  antigenic  determinant  of  pathogen   o   Makes  it  ineffective  in  establishing  infection   §   E.g.,  covers  region  of  virus  used  to  bind  cell  receptor     •   Agglutination    (clumping)   o   Antibody  cross-­‐links  antigens  of  foreign  cells  causing  clumping     §   Especially  effective  against  bacterial  cells     •   Preciptation   o   Antibody  cross-­‐links  circulating  antigens  (e.g.,  viral  particles)   o   Forms  antigen-­‐antibody  complex  that  becomes  insoluble  and  precipitates  out  of  body  fluids   o   Precipitated  complexes  recognized  by  phagocytes   •   Fc  region  (of  constant  region)  actions   o   Complement  fixation   §   Fc  region  can  bind  complement  for  activation  (classical  complement  activation)   o   Opsonization   §   Fc  region  makes  it  more  likely  target  cell  will  be  “seen”  by  phagocytic  cells   §   Some  phagocytes  have  receptors  for  these  Fc  regions   •   Bind  to  Fc  region  and  engulf  antigen  and  antibody   o   Activation  of  NK  cells   §   Fc  region  can  trigger  NK  cells  to  release  cytotoxins   §   This  destroys  abnormal  cells   22.9a  Immunologic  Memory   •   Memory  results  from  formation  of  a  long-­‐lived  army  of  lymphocytes  upon  immune  activation   o   Adaptive  immunity  activation  requires  contact  between  lymphocyte  and  antigen   §   There  is  lag  time  between  first  exposure  and  direct  contact   o   Activation  leads  to  formation  of  many  memory  cells  against  specific  antigen     22.9b  Measure  of  Immunologic  Memory   •   Initial  exposure  and  the  primary  response   o   Initial  exposure  can  be  active  infection  or  vaccine   o   Primary  Response:  antibody  production  to  first  exposure   §   Lag  or  latent  phase:  initial  period  of  no  detectable  antibody   §   Production  of  antibody:  plasma  cells  produce  antibodies   •   Occurs  within  1  to  2  weeks   •   Antibody  levels  peak,  then  decline  over  time   •   Subsequent  exposures  and  the  secondary  response   o   Next  exposure  can  occur  after  variable  length  of  time   o   Measurable  response  to  subsequent  exposure  is  the  Secondary  Response   §   Lag  or  latent  phase   •   Much  shorter  than  primary  response  due  to  memory  lymphocytes   §   Production  of  antibody   •   Antibody  levels  rise  rapidly   22.9a  Immunologic  Memory   •   With  subsequent  antigen  exposure   o   Many  memory  cells  make  contact  with  antigen  more  rapidly   o   Produce  powerful  secondary  response   §   Pathogen  typically  eliminated  before  disease  symptoms  develop   §   E.g.,  person  who  develops  measles  will  not  have  it  again,  even  if  exposed   •   Virus  eliminated  by  memory  T-­‐  and  B-­‐lymphocytes,  antibodies  before  causing  harm   o   Vaccines  are  typically  effective  in  developing  memory   22.9c  Active  and  Passive  Immunity   •   Active  Immunity   o   Results  from  direct  encounter  with  pathogen   §   Occurs  naturally  by  direct  exposure  to  antigen   §   Can  occur  artificially  through  exposure  through  vaccine   o   Memory  cells  against  specific  antigen  are  formed   22.9c  Active  and  Passive  Immunity   •   Passive  Immunity  obtained  from  another  individual   o   Natural  passive  immunity  arises  from  transfer  of  antibodies  from  mother  to  fetus  (through   placenta  or  milk)   o   Artificial  passive  immunity  occurs  when  serum  containing  antibodies  transferred  from  one   person  to  another   §   E.g.,  antibodies  to  snake  venom  can  be  transferred  this  way   o   Neither  form  of  passive  immunity  produces  memory  cells   §   Lasts  only  as  long  as  antibody  proteins  present     Clinical  View:  Pus  and  Abscesses   •   Pus     o   Contains  destroyed  pathogens,  dead  leukocytes,  macrophages,  cellular  debris   o   Removed  by  lymphatic  system  or  through  skin   o   If  not  completely  cleared,  may  form  abscess   §   Pus  walled  off  with  collagen  fibers   §   Usually  requires  surgical  intervention  to  remove       Clinical  View:  Organ  Transplants  and  MHC  Molecules   •   Transfer  of  organ  from  one  individual  to  another     o   E.g.,  kidney,  liver,  heart   •   Individuals  tested  prior  to  donation  for  MHC  antigens  and  ABO  group   o   No  two  individuals  with  exactly  same  MHC  molecules   •   Components  of  innate  and  adaptive  immune  system   o   Attempt  to  destroy  transplanted  tissue   o   Recipient’s  immune  system  suppressed  with  drugs   Clinical  View:  Vaccinations   u   Weakened  or  dead  microorganism  or  component   u   Stimulate  immune  system  to  develop  memory  B-­‐lymphocytes   u   Provide  relatively  safe  means  for  initial  exposure  to  microorganism   u   If  later  exposed,  secondary  response  triggered   u   Immune  system  response  predominantly  from  the  humoral  branch   u   May  provide  lifelong  immunity   Clinical  View:  Hypersensitivities   u   Acute  hypersensitivity,  Allergy   u   Overreaction  of  immune  system  to  a  noninfectious  substance,  Allergen   u   E.g.,  pollen,  latex,  peanuts   u   May  cause  multiple  symptoms   u   Runny  nose  and  watery  eyes   u   Red  welts  and  itchy  skin  (hives)   u   Labored  breathing  and  coughing  (allergic  asthma)   u   Vomiting  and  diarrhea   u   Systemic  vasodilation  and  inflammation   u   May  go  into  anaphylactic  shock   Clinical  View:  HIV  and  AIDS   u   Acquired  immunodeficiency  syndrome   u   Life-­‐threatening  condition   u   Result  of  human  immunodefiency  virus   u   Infects  and  destroys  helper  T-­‐lymphocytes   u   Resides  in  body  fluids  of  infected  individuals   u   Can  be  transmitted  by  intercourse,  needle  sharing,  breastfeeding   u   Prevention  through  safe  sex   u   No  cure  for  HIV   u   Treatments  alleviate  symptoms  and  help  prevent  spread    


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