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Immune System PowerPoint Notes

by: Victoria Hills

Immune System PowerPoint Notes Biol 2230-001

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Here is all the information covered on each of the slides for the immune system powerpoint notes.
Human Anatomy & Physiology II
Dr. John Cummings
Class Notes
Human, anatomy, Physiology, Clemson, Cummings, immune, system, power, point, Slides
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This 17 page Class Notes was uploaded by Victoria Hills on Thursday March 3, 2016. The Class Notes belongs to Biol 2230-001 at Clemson University taught by Dr. John Cummings in Fall 2015. Since its upload, it has received 26 views. For similar materials see Human Anatomy & Physiology II in Biology at Clemson University.


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Date Created: 03/03/16
Clemson  University     Spring  2016   Immune  System  PowerPoint   Slide  1:  Immune  System   • Immune  system  doesn’t  have  numerous  organs  working  together  but  instead   it  has  functions  working  together  that  bring  about  an  immune  response   • Immune  System  can:   -­‐ Prevent  the  entry  of  pathogens  into  the  body   -­‐ Prevent  the  spread  of  pathogens  throughout  the  body  by  keeping  the   pathogenic  problem  to  one  area  +  killing  it  if  there  was  a  breech     • Pathogen:  A  disease  causing  agent     • Antigen:  Foreign  thing  that  the  body  wants  to  get  rid  of  it  enters  the  body   (Can  include  pathogens)   Slide  2:  Immune  Systems:  Nonspecific  Immune  System   • AKA  innate  immune  system   • Part  of  the  immune  system  that  attacks  anything  foreign     • Consists  of  external  body  membranes  and  can  include  inflammatory   response     • Inflammatory  Response:   -­‐ Ex:  Cut  on  the  body   o The  inflammatory  response  is  activated  since  the  membrane  of  the   skin  was  cut  and  some  substances  were  able  to  enter  through  the   breech   o Inflammatory  response  works  to  try  to  keep  the  foreign   substances  localized  to  that  area  so  that  they  don’t  spread  to  the   rest  of  the  body     -­‐ Ex:  Mosquito  Bite:   o Can  see  where  the  inflammatory  response  keeps  the  foreign   substance  localized   Slide  3:  Immune  Systems:  Specific  Immune  System   • AKA  adaptive  immune  system     • Individual  cells  respond  to  certain  and  specific  foreign  substances   • Includes  B  and  T  lymphocytes   • Ex:  There  are  B  lymphocytes  that  only  respond  to  Staphylococcus   Slide  4:  Superficial  Nonspecific  Defenses:  Skin   • Unbroken  epidermis  is  a  great  barrier  to  antigens/pathogens   • Epidermal  tissue  does  not  have  a  blood  supply  à  Means  that  the  skin  is   made  up  of  squamous  epithelium  that  is  mostly  dead     • Have  protein  layers  stacked  up  on  top  of  each  other  =  barrier   Slide  5:  Superficiual  Nonspecific  Defenses:  Mucous  Membranes   • A  mucosal  lining  can  be  found  on  all  internal  body  cavities  that  is  composed   of  epithelial  tissue  and  also  creates  a  physical  barrier   • Mucous  membranes  also  secrete  mucous  that  act  like  a  trap  so  that  any   foreign  substances  inside  the  body  can  be  stuck  in  the  cavities  of  the  mucous   membranes   • Mucous  secretions  create  an  acidic  environment  à  Foreign  cells  can  be   destroyed  by  the  acids   • Production  of  protein  digesting  enzymes  that  are  able  to  break  down   foreign  substances  with  a  protein  coat   • Some  mucous  membranes  can  produce  lysozymes:  Enzymes  in  lysosomes   that  are  able  to  break  apart  foreign  substances  (Can  be  found  in  tears,  saliva,   etc.   *Overall:  Skin  and  mucous  membranes  function  to  keep  foreign  substances  out  of   the  body,  but  the  barriers  can  be  breeched  so  there  is  a  need  for  additional   nonspecific  mechanisms     Slide  6:  Internal  Nonspecific  Defenses:  Phagocytes   • Phagocytosis:  Phagocytic  cells  surround  something  that  is  foreign  by   extending  their  cytoplasm  and  bring  it  inside  a  vacuole  to  destroy  it   • Free  phagocytes:  Found  in  circulation   • Fixed  phagocytes:  Found  in  the  lymph  organs  that  hang  out  in  the  reticular   cells   • Phagocytes:     a) Macrophages:   -­‐ Derived  from  monocytes  that  escaped  from  circulation  through   diapedesis     b) Neutrophils:   -­‐ Continuously  in  circulation  in  the  blood  stream   -­‐ Become  phagocytic  when  they  bind  to  a  foreign  cell   c) Eosinophils:   -­‐ Continuously  in  circulation  in  the  blood  stream   -­‐ Attack  internal  parasitic  worms   Slide  7:  Internal  Nonspecific  Defenses:  Mast  Cells   • Mast  cells  are  somewhat  phagocytic  but  are  different  than  phagocytes  in  the   way  they  find  the  foreign  substance  and  bring  it  inside  the  mast  cell   • Have  specific  receptors  that  are  non-­‐specific  à  Means  that  mast  cells  can   bind  to  a  number  of  different  things  that  then  digest  the  bound  components   and  kill  them   • Mostly  bind  to  bacteria     Slide  8:  Internal  Nonspecific  Defenses:  Natural  Killer  Cells   • Natural  killer  cells  are  a  class  of  lymphocytes  (In  addition  to  the  T  and  B   lymphocytes)  that  circulate  in  the  blood  stream  so  that  when  they  encounter   anything  abnormal,  they  automatically  kill  it   • Lyse  foreign  substances  and  not  phagocytize  them     • Attack  cancerous  cells  or  cells  infected  by  a  virus   • Cancerous  cells  are  abnormal  cells   • Virus  within  a  cell:  Parts  of  the  virus  appear  on  the  surface  of  the  body  cell  so   that  it  looks  weird  à  Therefore,  natural  killer  cells  attack  any  cell  that  does   not  look  normal     Slide  9:  Internal  Nonspecific  Defenses:  Inflammation   • Inflammation  is  the  result  of  the  dilation  of  capillaries  that  become  larger  and   porous   • 4  Symptoms  of  Inflammation:   a) Redness:   -­‐ Capillaries  are  dilated  so  more  blood  is  able  to  rush  to  the  site  of  damage   -­‐ Blood  pigment  is  red  so  because  there  is  more  blood,  the  area  will  appear   more  red   b) Swelling:   -­‐ When  the  capillaries  dilate,  they  become  more  permeable   -­‐ Fluids  leak  out  of  the  bloodstream  and  accumulate  as  a  result  to  create   swelling   c) Heat:   -­‐ Blood  is  warmer  than  the  rest  of  the  body   -­‐ Therefore,  when  blood  accumulates  in  one  spot  à  That  location  will  feel   much  warmer  than  the  rest  of  the  body   d) Pain:   -­‐ As  fluid  accumulates  at  the  site  of  inflammation,  it  causes  pressure  that   activates  pain  receptors   • Purpose  of  inflammation:  By  delivering  more  blood  to  the  site  of  damage,   more  most  mast  cells,  natural  killer  cells,  phagocytic  cells,  etc.  can  be   delivered  to  fight  off  foreign  substances  in  a  non-­‐specific  fashion  +  keeps  the   foreign  substances  from  leaving  that  location   Slide  10:  Internal  Nonspecific  Defenses:  Antimicrobial  Proteins   • Antimicrobial  Protein:  Attack  microorganisms  by  destroying  them  or   interfering  with  their  reproduction  (Like  with  viruses)   • Interferon:   -­‐ Antimicrobial  protein  secreted  by  a  cell  infected  by  a  virus  in  order  to   signal  neighboring  cells  to  induce  changes  to  protect  themselves  form  the   virus     -­‐ Disrupts  viral  replication  in  neighboring  cells  so  that  they  can’t   reproduce   • Complement  System:   -­‐ Involves  more  than  20  different  proteins  that  function  in  complement   -­‐ Blood  proteins  that  circulate  in  the  blood     -­‐ If  they  become  activated,  complement  system  (proteins)  promote   inflammation     -­‐ Some  complement  proteins  can  cause  lysis  to  occur     Slide  11:  Internal  Nonspecific  Defenses:  Fever   • Fever:  Elevation  of  body  temperature  à  Systemic  response   • Interferes  with  replication  of  foreign  cells   Slide  12:  Phagocytic  Mechanism  (Phagocytosis)   • Phagocyte  recognizes  pathogen’s  carbohydrate  surface  markers   -­‐ Phagocytes  are  able  to  differentiate  between  body  cells  and  pathogens   because  “Self”  markers  on  body  cells  are  MHC  (Major  histocompatibility   complex)  and  pathogens  do  not  have  the  MHC  self  marker     • *(Phagocytes  located  in  the  body  and  in  interstitial  space  and  lymphatic   organs  are  not  active  until  they  encounter  a  foreign  cell)   • Opsonization:     -­‐ Enhances  the  recognition  of  a  foreign  cell   -­‐ Antibodies  that  attach  to  the  foreign  cell  are  able  to  flag  it  and  make  it   easier  to  be  found  and  destroyed   • Adherence:  Phagocytic  cells  attach  to  the  foreign  cell  by  sending  out   cytoplasmic  extensions  that  adhere  to  the  pathogen     • After  adherence  to  the  pathogen,  the  phagocyte  brings  the  foreign  cell  into  its   own  body  in  vacuole  à  Phagocyte  +  pathogen  inside  =  phagosome   • Phagosome  combines  with  lysosomes  (Carry  lysozymes)  to  forms  a   phagolysosome  so  that  the  lysozymes  break  down  the  pathogen   • Lysozymes  can  be  aided  by  respiratory  burst  (Additional  chemicals)  in   breaking  down  pathogen   • Breakdown  products:   -­‐ Residual  bodies  still  contained  within  the  phagosome  that  are  expelled   out  of  the  phagocyte  and  filtered  through  the  blood  and  lymph  to  be   expelled  as  waste   Slide  13:  Natural  Killer  Mechanism   • Natural  killer  cells  detect  body  cells  that  have  become  cancerous  or  infected   through  lack  of  “Self”  (MHC)  markers  or  by  the  presence  of  certain  sugars   • Key  that  natural  killer  cells  detect  problems  with  body  cells  and  NOT  foreign   cells   • Adherence  of  a  natural  killer  cell  to  an  abnormal  body  cell  activates  the   natural  killer  cell  to  release  perforins  (proteins)  that  lead  to  a  cytotoxic  T   cell  process  (Both cT  and  natural  killer  cells  use  the  same  key  mechanism— discussed  later)  à  natural  killer  cells  bore  holes  into  the  plasma  membrane   to  disrupt  the  cell  and  cause  it  to  become  fractured   • Channels  in  the  plasma  membrane  of  the  target  cells  result  to  allow  the   formation  of  holes  in  the  nuclear  membrane  as  well  so  that  the  nucleus   disintegrates     Slide  14:  Inflammatory  Mechanism   • Macrophages  have  toll-­‐like  receptors  that  are  non-­‐specific  on  their   surfaces  that  recognize  pathogens   • When  the  toll-­‐like  receptors  bind  to  the  pathogen,  cytokines  are  released     • Cytokines  promote  inflammation  à  signaling  capillaries  to  dilate   • Cytokines  also  attract  white  blood  cells  wherever  they  are  produced  (Exhibit   positive  chemotaxis)   • Activation  of  the  toll-­‐like  receptors  on  a  macrophage  causes  other  cells  in  the   same  area  to  release  other  chemicals  that  are  inflammatory  mediators  such   as  histamines,  prostaglandins,  or  any  sort  of  chemical  with  a  localized  change   or  effect     • Cytokines  signal  blood  vessels  in  the  injured  area  to  dilate  and  increase   permeability  à  hyperemia:  Excessive  blood   • Increased  permeability  allows  the  plasma  to  leave  the  capillary  and  move   into  the  interstitial  space  à  Exudate  (Fluid  and  clotting  factors  containing   antibodies  that  have  left  circulation  and  that  accumulate  at  the  site  where  the   capillary  is  most  permeable)   • When  exudate  accumulates  this  leads  to  swelling,  which  is  also  known  as   edema   • Edema  functions  and  effects:   -­‐ Helps  to  dilute  the  foreign  substances  à  more  exposure  for  the  immune   system  to  be  more  efficient  in  detecting  the  foreign  substances   -­‐ Brings  oxygen  and  nutrients  to  activate  other  substances  like  enzymes   -­‐ Carries  clotting  proteins  to  plug  breaks  in  a  barrier  with  a  clot   Slide  15:  Results  of  Inflammation   • Injured  cells  release  leukocytosis-­‐inducing  factors  à  Cause  neutrophils  to   be  released  from  the  red  bone  marrow   • Leukocytosis:  Higher  than  normal  numbers  of  neutrophils  in  the  blood   Slide  16:  Results  of  Inflammation   • Loss  of  fluids  slows  blood  flow  locally   • Flow  of  fluids  leaking  out  of  the  bloodstream  à  low  blood  pressure  à   ultimately  slows  down  blood  flow   Slide  17:  Results  of  inflammation   • Neutrophils  are  able  to  accumulate  at  the  site  of  damage  due  to  the  slow   blood  flow   • Some  neutrophils  will  be  grabbed  and  held  near  the  site  of  damage  due  to   endothelial  cells  from  inside  the  wall  of  a  capillary  secreting  selectin   • Margination:  The  process  of  holding  neutrophils  at  the  wall  of  a  capillary   near  the  site  of  damage   • Neutrophils  held  on  the  cell  wall  of  capillaries  near  the  site  of  damage  will   then  diapedese  and  escape  the  capillaries     • Neutrophils  are  phagocytic  cells  that  attack  foreign  substances   Slide  18:  Results  of  Inflammation   • Inflammatory  chemicals  (Includes  selectins  and  mediator  chemicals)  act  as   chemotactic  agents  that  mostly  attract  neutrophils  to  an  area  of  damage   • Once  neutrophils  have  escaped  the  walls  of  the  capillaries,  monocytes  follow   out  (Diapedese)  of  the  capillaries  as  well  and  become  macrophages     • Macrophages  have  more  lysosomes  (Full  of  enzymes  that  break  substances   apart)   Slide  19:  Interferon  Mechanism   • Cells  infected  by  a  virus  release  interferons  (IFN)   • Interferons  diffuse  into  neighboring  cells  that  causes  them  to  synthesize  PKR   protein  that  interferes  with  viral  replication  through  prevention  of  use  of  the   host  cell’s  machinery     • Interferons  also  activate  macrophages  and  natural  killer  cells   Slide  20:  Complement  System  Mechanism  I   • Antibodies  bind  to  antigens/pathogens  (Opsonization  has  occurred)   -­‐ Antibodies  binding  to  specific  antigens  is  part  of  a  specific  immune   response  that  can  invoke  a  non-­‐specific  action  (Here  the  complement   proteins)   • Complement  proteins  bind  to  antibody-­‐pathogen  complexes   • Lysis,  phagocytosis,  and  inflammation  result     • Complement  proteins  circulate  in  the  plasma  portion  of  the  blood  and  wait  to   be  called  to  action   Slide  21:  Complement  System  Mechanism  II   • Complement  proteins  bind  directly  to  the  polysaccharide  molecules  on  the   antigen/pathogen  (Skip  antibody  attachment  step)   • Lysis,  phagocytosis,  and  inflammation  result   Slide  22:  Fever  Mechanism   • Leukocytes  and  macrophages  exposed  to  pathogens  secrete  pyrogens   • Pyrogens  signal  the  hypothalamus  to  elevate  body  temperature     • By  increasing  whole  body  temperature,  the  availability  of  iron  and  zinc  is   reduced  which  are  important  components  that  bacteria  used  to  divide  à     Bacteria  eliminated  as  a  result  since  they  aren’t  able  to  divide   • Pyrogens  also  elevate  metabolic  activity  à  One  way  of  producing  the   necessary  heat     -­‐ Heat  is  produced  from  shivering  when  you  feel  cold  even  though  the  body   temperature  can  be  at  102+  degrees  F     -­‐ Then  fever  breaks   Slide  23:  Antigen   • French   • Any  substance  that  promotes  an  immune  response  (Anything  foreign)   Slide  24:  Antigenic  Properties   • Antigens  demonstrate  immunogenicity   • Reactivity:   -­‐ Markers  on  the  surface  of  cells  are  able  to  interact  with  antibodies  or   lymphocytes   -­‐ Antigens  promote  interactions  with  immune  cells  due  to  their  reactive   components  (Antigenic  determinants)   • Antigenic  determinants:  Reactive  parts  of  a  an  antigen  that  gives  it   immunogenicity     Slide  25:  Major  Histocompatibility  Complex   • Body  cells  have  genetically  determined  markers  on  their  surface  =  “self”   antigens  that  are  also  known  as  MHC  markers   • MHC  markers  are  not  immunogenic  to  us  (Not  reactive/immune  system   wouldn’t  attack  them)     • Our  own  MHC  markers  would  be  immunogenic  to  other  individuals  except   for  those  with  identical  twins     Slide  26:  Characteristics  of  Specific  Immunity   • AKA  adaptive  immunity   • Pathogen  specific   • Specific  immunity  is  not  immediately  active  à  When  specific  immune  cells   come  in  contact  with  the  specific  antigen,  there  is  a  delay  before  the  specific   immune  cells  become  fully  active     • Systemic  with  specific  immune  cells  circulating  the  body  all  the  time   scanning  for  specific  pathogens   • Provides  memory:  The  activation  of  specific  immune  cells  will  cause  the   production  of  more  of  those  cells  that  will  then  interact  with  the  antigen   faster  the  next  time  it  encounters  it  (Time  lag  is  shortened  as  well)   Slide  27:  Pathways:  Humoral   • Humoral:  Fluid   • Specific  immune  cells  interact  with  antigens  that  are  free  floating  (Found  in   the  blood  stream  and  circulating  the  body)   • Humoral  pathway  is  an  antibody-­‐mediated  pathway  since  antibodies  detect   the  free  floating  pathogens  (Uses  B  lymphocytes)   • Antigens  +  antigenic  determinants  on  the  surface  of  an  antigen  along  with  the   antibodies  are  specific   • Antibodies  do  NOT  kill  the  specific  antigen  directly  à  It  is  marked  so  that   another  immune  cell  can  kill  it,  such  as  complement  proteins  or  phagocytic   cells   • In  general,  a  specific  immune  response  is  able  to  activate  a  non-­‐specific   immune  response   • Main  point:  Humoral  pathway  marks  antigens  for  destruction     Slide  28:  Pathways:  Cell-­‐Mediated   • Pathway  where  one  of  our  body  cells  has  become  infected  so  the  T   lymphocytes  will  attack  and  kill  the  infected  body  cell   • This  process  is  similar  to  that  of  the  natural  killer  cells,  except  that  the   natural  killer  cells  attack  anything  à  Each  T  lymphocyte  in  the  cell-­‐mediated   pathway  can  only  bind  to  a  certain  type  of  infectious  agent   • Main  point:  Cell-­‐mediated  pathway  kills  infectious  agents  directly  by  cell   lysis     Slide  29:  Lymphocyte  Production   • Humoral:  B  lymphocytes   • Cell-­‐mediated:  T  lymphocytes   • All  lymphocytes  are  produced  by  stem  cells  in  the  red  bone  marrow     • Immature  lymphocytes  are  virtually  identical  until  they  mature   • Immature  lymphocytes  migrate  to  the  bone  marrow  or  thymus  (Primary   lymph  organs)  to  become  immunocompetent  (Point  where  receptors  are   required  to  interact  with  a  specific  antigen  and  its  antigenic  determinants)   Slide  30:  Lymphocyte  Production   • T  lymphocytes:  Immunocompetent  in  the  thymus   Slide  31:  Lymphocyte  Production   • B  lymphocytes:  Immunocompetent  in  the  bone  marrow     **Immunocompetent  T  and  B  lymphocytes  still  have  to  remain  in  secondary   lymph  organs  (Spleen,  lymph  nodes,  etc.)  until  they  mature  and  even  when  they   are  mature,  they  are  not  fully  functional  until  they  bind  to  an  antigen   Slide  32:  Lymphocyte  Production:  Recap   • Produced  by  stem  cells  in  red  bone  marrow   • T  cells  become  immunocompetent  in  thymus   • B  cells  become  immunocompetent  in  bone  marrow   • Immunocompetent  cells  mature  in  secondary  lymphoid  organs   Slide  33:  Lymphocyte  Production:  Recap   • Not  fully  functional  until  bound  with  antigen   Slide  34:  Antigen-­‐Presenting  Cells   • Engulfs  pathogen  and  presents  its  fragments  as  antigens   Slide  35:  Cell-­‐Mediated  Immune  Response   • Review:   -­‐ 1  line  of  defense  (Non-­‐specific):  Protective  barrier   -­‐ 2  line  of  defense  (Non-­‐specific):  Keeping  the  antigen  in  one  spot  +   attempting  to  eliminate  it   rd -­‐ 3  line  of  defense  (Specific):  Specific  approach  where  the  specific   immune  system  tries  to  target  invaders  and  kill  them     -­‐ 4  line  of  defense  (Specific):  After  body  cells  have  become  infected,  the   immune  system  has  to  attack  its  own  altered  body  cells  and  lyse  them   • Non-­‐specific  immune  system  keeps  working  even  though  it  may  not  initially   solve  the  pathogenic  problem   Slide  36:  Antigen  Challenge   • Antigen  challenge:  First  encounter  between  a  specific  naïve   immunocompetent  lymphocyte  and  antigen     • Review:   -­‐ Lymphocytes  are  produced  in  red  bone  marrow  à  lymphocyte  à   primary  lymphoid  organ  (Bone  marrow  or  thymus)  à  Immucompetency   achieved   -­‐ Cells  producing  proteins  due  to  genes  are  expressed  on  the  surface  of  the   cell  that  become  the  receptors  specific  for  their  specific  antigens   • Immunocompent  lymphocyte:  Can  interact  with  specific  antigens  but  won’t   yet   • Naïve  competent  cell:  Ready  to  interact  with  specific  antigen  but  hasn’t  yet   Slide  37:  Primary  Humoral  Response   • Antigens  in  the  humoral  pathway  are  free  floating  in  the  fluids  in  the  plasma   and  lymph   • Antigens  bind  with  surface  receptors  on  naïve  immunocompetent  B   lymphocytes   • When  the  specific  antigen  and  immunocompent  B  lymphocyte  connect  à  B   lymphocyte  becomes  active  and  the  clonal  sectional  process  is  stimulated   • Clonal  Selection:  When  the  cell  grow  and  multiplies  to  produce  clones  of   that  particular  lymphocyte  with  identical  receptors  for  that  specific  antigen     • Most  clones  produce  and  become  plasma  cells  that  produce  antibodies   (Mark  specific  antigen  for  destruction)   • Some  clones  instead  of  producing  plasma  cells  and  therefore  antibodies  are   stored/remain  as  memory  cells  that  wait  to  respond  to  another  of  the  same   infection  in  the  future  (Secondary  humoral  response)   • Primary  Humoral  Response:  The  very  first  encounter  between  a  naïve   immunocompetent  lymphocyte  and  its  specific  antigen     Slide  38:  Secondary  Humoral  Response   • Refers  to  any  subsequent  exposure   • Same  mechanism  as  primary  humoral  response  but  is  much  more  rapid  and   produces  a  lot  more  antibodies  (Higher  titer-­‐  concentration  of  antibodies)   that  last  longer  (For  months)     • Figure:     a) Primary  humoral  response  to  antigen  X:  Takes  about  7-­‐10  days  for  us   to  reach  maximum  titer  (maximum  number  of  antibodies)  that  lasts  for   about  4-­‐5  days  that  then  declines     -­‐ AKA  primary  response  characteristics  include,  lag,  limited  antibody   production  and  short  duration   b) Secondary  humoral  response  to  antigen  X:  More  rapid,  more   antibodies  produced  (higher  titer)  and  last  longer     c) Exposure  to  antigen  Y  is  shown  along  with  secondary  exposure  to   antigen  X  so  that  primary  humoral  response  is  induced  again  for  antigen   Y   Slide  39:  Sources  of  Humoral  Immunity   • Refers  to  how  to  get  antibodies  present  in  the  body  for  humoral  responses     • Active  Immunity:   -­‐ Our  own  system  makes  the  antibodies  due  to  a  full-­‐blown  antigen  being   present   -­‐ AKA:  Antigen  activate  B  lymphocytes  to  produce  plasma  to  produce   antibodies   • Passive  Immunity:   -­‐ Obtaining  antibodies  from  a  source  other  than  our  own  bodies   -­‐ AKA:  Antibodies  were  produced  somewhere  else   • Natural  and  artificial  immunity     • Combinations:   a) Natural  Active  Immunity:   -­‐ Similar  to  active  immunity  in  that  we  had  to  have  been  infected  by  a  full-­‐ blown  pathogen  to  induce  production  of  antibodies  by  our  own  body   b) Natural  Passive  Immunity:   -­‐ Ex:  Antibodies  are  produced  by  the  mother  that  pass  across  the  placenta   and  are  given  to  the  baby   -­‐ Ex:  Antibodies  produced  by  the  mother  that  are  passed  to  the  baby   through  breast  milk   c) Artificial  Active  Immunity:   -­‐ Immunizations  are  where  an  attenuated  (weakened)  antigen  is  injected   so  that  it  won’t  make  you  sick  but  it  still  activates  an  immune  response  so   that  the  body  can  make  its  own  antibodies   d) Artificial  Passive  Immunity:   -­‐ Vaccines  are  where  antibodies  (Called  immunoglobulins  here)  are   injected  into  another  body     -­‐ Antibodies  have  been  made  to  fight  off  infections  for  you   Slide  40:  Antibody  Structure   • Antibodies  are  complex  proteins  à  Made  up  of  4  subunits   • Also  called  immunoglobulins  or  gamma  globulins   • 2  identical  light  chains:  Variable  region  à  Have  antigen  binding  sites  to   determine  what  antigen  the  antibody  will  bind  to     • 2  identical  heavy  chains:  Constant  region  à  Same  in  each  antibody  and   dictates  how  an  antigen  will  be  destroyed     • Some  constant  regions  will  bind  complement  proteins  that  will  lyse  cells  and   kill  them,  attract  phagocytic  cells,  or  simply  mark  the  antigen  for  destruction   (Ex:  By  phagocytosis  with  a  dendritic  cell  or  macrophage)       Slide  41:  Classes  of  Antibodies:  IgD,  IgG,  and  IgE   • Most  antibodies  are  single  units  with  light  (short)  chains  that  bind  the   antigen  and  heavy  (long)  chains  that  destroy  the  antigen   • IgD:   -­‐ Receptor  on  the  surface  of  a  B  lymphocyte   -­‐ Is  incorporated  into  the  B  lymphocyte  to  make  it  immunocompetent   • IgG:   -­‐ Most  abundant  of  all  antibodies   -­‐ Main  antibody  present  in  the  late  portion  of  the  primary  and  secondary   response   -­‐ There  is  a  longer  lag  time  in  the  production  of  IgG  than  others  because   they  have  to  get  to  the  end  of  the  responses  before  circulating  in  the   plasma  to  fight  off  antigens   -­‐ Can  invoke  passive  immunity  by  crossing  the  placenta   -­‐ Bind  to  specific  antigen  and  use  complement  proteins  and  otherwise   exhibit  phagocytosis  (On  the  heavy  chains)   • IgE:   -­‐ Don’t  have  many  IgE   -­‐ Increase  seen  with  individuals  with  allergies   -­‐ Can  bind  to  mast  cells  that  have  engulfed  a  foreign  substance  and  tells   basophils  to  release  histamine  granules   -­‐ Overalll:  IgE  cause  the  production  of  histames  that  causes  IgE  to  replicate   • IgG:IgE  à  IgE  should  be  far  more  numerous,  but  if  there  isn’t  much  for  the   immune  system  to  do,  the  IgE  will  respond  to  allergens   • In  order  to  control  allergies,  suppression  of  IgE  leads  to  suppression  of   histamine  response   Slide  42:  Classes  of  Antibodies:  IgA   • IgA:     -­‐ Dimer:  2  units  (monomers)  are  attached  together  à  Have  4  receptor   sites  (Instead  of  the  usual  2)  on  the  variable  region  and  constant  region   -­‐ Tend  to  accumulate  in  mucous  and  other  body  secretions   -­‐ Binding  to  their  specific  antigens  prevents  the  antigens  from  attaching  to   epithelial  cells   Slide  43:  Classes  of  Antibodies:  IgM   • IgM:   -­‐ Pentamer:  5  monomers  are  attached  together  à  Have  10  receptor  sites   -­‐ First  antibody  secreted  by  plasma  cells  during  a  primary  immune   response  to  help  prevent  the  spread  of  the  foreign  substance  (IgG  are   produced  later  in  the  response  and  have  more  of  these  than  IgM)   -­‐ Can  be  used  in  a  diagnostic  test  to  see  if  an  individual  has  had  a  recent   infection  or  an  older  infection   -­‐ Readily  fixes  and  activates  complement   -­‐ Promotes  agglutination:   o Agglutination:  Antigens  bound  to  IgM  clump  together  and  are   isolated  in  one  spot  so  that  non-­‐specific  cells  (Ex:  Natural  killer   and  phagocytic  cells)  are  drawn  towards  that  area   Slide  44:  Antibody  Functions   • Formation  of  antigen-­‐antibody  complex  à  Mark  antigens  for  destruction   through  variable  site   • Provides  site  for  binding  of  complement  proteins  through  the  constant   region     -­‐  Complement  protein  fixation  à  Secretion  of  perforins  that  cause  lysis  of   cells  (Or  due  to  another  cytolytic  chemical)   • Blocks  sites  on  pathogens  so  they  won’t  be  able  to  bind  to  other  cells  in  the   bodyà  Neutralization  process  in  neutralizing  the  antigen  so  it  won’t  attack   our  bodies  (Ex:  IgA  function)   • Cause  clumping  of  antigen-­‐containing  cells  that  allows  greater  phagocytosis   efficiency  in  keeping  the  antigens  in  one  spot  à  Sometimes  they  can  still  be   traveling  throughout  the  body   • Cause  clumping  of  soluble  antigen  molecules:  It’s  even  better  to  precipitate   out  the  antigens  so  they  don’t  have  to  travel  as  much  à  Again,  taking  the   soluble  antigen  molecules  out  of  solution  helps  so  that  phagocytes  can  have   better  access  to  the  antigens   Slide  45:  Monoclonal  Antibodies   • Commercially  produced  antibodies   • Process:   -­‐ Infect  another  organism   -­‐ Organism  produces  antibodies   -­‐ Collect  blood  serum  or  plasma     -­‐ Extract  antibodies  to  be  used  for  vaccines,  research,  cancer  treatment,  etc.     Slide  46:  Cell-­‐Mediated  Immune  Response   • Part  of  B  lymphocytes  functions  to  attract  phagocytes  to  infected  body  cells   in  addition  to  trying  to  eliminate  free  floating  antigens  in  the  humoral   response   • Cell-­‐mediated  response  has  to  do  with  an  infected  body  cells  à  A  naive   immunocompetent  T  cell  is  going  to  bind  with  one  of  the  antigen  infected   body  cells  that  does  not  have  a  normal  MHC  “self”  marker   • T  lymphocyte  with  the  specific  receptor  will  bind  to  that  infected  cell  (AKA  T   cell  has  bound  to  an  antigen  presenting  cell)   • Next,  a  second  binding  has  to  occur  where  the  other  arm  has  to  bind  to   something  else  to  release  costimulatory  signals  that  help  activate  T   lymphocytes   • Key:  After  the  T  lymphocyte  has  bound  to  the  infected  cell  with  one  arm   and  the  binding  of  something  to  the  other  arm  has  occurred  to  allow  the   release  of  costimulatory  cells,  the  T  lymphocyte  has  then  been  activated   -­‐ This  is  different  than  B  lymphocytes  where  when  a  B  lymphocytes   attaches  to  an  antigen  it  is  activated   • Activated  T  cell  will  go  through  clonal  selection  to  produce  more  T   lymphocytes  with  receptors  for  that  specific  antigen  +  some  clones  will   remain  as  memory  cells  for  future  encounters  of  the  same  infection   • *T  lymphocytes  do  NOT  produce  antibodies  but  they  attack  altered  body  cells     Slide  47:  T  Cells   • There  is  more  than  one  type  of  T  cell   • CD4  and  CD8  cells  differentiation  is  due  to  differences  of  markers   (glycoproteins)  on  the  surfaces  of  these  T  cells  that  ultimately  affect  what   antigens  they  can  bind  to     Slide  48:  T  Cell  Activators   • CD4  Cells:  T4  Cells  à  Helper  T  cells   • CD8  Cells:  T  Cells  à  Cytotoxic  T  cells/Killer  T  cells   8 • Differences  between  the  2  T  cells:  Antigens  they’ll  attach  to  and  what   activates  them   • Two  classes  of  altered  MHC  “self”  markers  on  body  cells  that  activate  T  cells:   a) Class  I  MHC  Protein-­‐Linked  Antigens:  CD8   -­‐ Endogenous  (Produced  by  the  body)     -­‐ Antigen  part  comes  from  the  body  itself     -­‐ A  virus  affects  a  body  cell  that  has  MHC  +  part  of  virus  (antigen)  present   on  the  surface   -­‐ Cancerous  cells  included   -­‐ All  body  cells  can  produce  MHC  except  for  red  blood  cells   -­‐ Any  body  cell  that  is  infected  will  put  antigen  on  surface  of  cell   -­‐ T 8  (CD8)  or  cytotoxic  cells  interact  with  class  I  MHC   b) Class  II  MHC  Protein-­‐Linked  Antigens:  CD4   -­‐ Exogenous  (Antigen  part  is  produced  outside  of  the  body  and  is  foreign)   -­‐ Found  on  phagocytic  cells  that  engulf  bacteria   -­‐ T 4  (CD4)  or  helper  T  cells  interact  with  class  II  MHC   Slide  49:  Antigen  Binding   • T  cell  antigen  receptors  bind  to  antigen-­‐MHC  complex     Slide  50:  Co-­‐stimulators   • Then  there  has  to  be  a  second  step  where  there  binding  to  other  receptors  on   APC  (Antigen  presenting  cells)  that  causes  the  production  of  costimulatory   signals  such  as  cytokines  and  interleukins     • Each  costimulatory  signal  promotes  a  different  response  that  either   facilitates  or  disables  activation   • T  lymphocyte  is  activated  after  antigen  binding  and  constimulatory  signal   release   Slide  51:  Cell-­‐Mediated  Immune  Response   • T  cell  binds  with  antigen  infected  body  cell   • Co-­‐stimulatory  signals  are  present   • T  cell  is  activated   • Clones  are  produced   • Some  clones  become  memory  cells   Slide  52:  Types  of  T  Cells:  Cytotoxic  T  Cells   • Cytoxic  T  cell  =  CD8  cell   • Directly  attacks  and  kills  cells  with  Class  I  MHC     • Therefore,  once  the  CD8  cell  attaches  to  the  specific  antigen  and  the   costimulatory  signals  are  present,  the  infected  body  cell  is  lysed  and  broken   up     Slide  53:  Types  of  T  Cells:  Helper  T  Cells   • Helper  T  Cells  =  CD4  cells  that  bind  to  Class  II  MHC  (Phagocytic  cell  engulfed   something  foreign)   • One  the  helper  T  cells  have  attached  to  the  antigen  and  the  co-­‐stimulatory   signals  are  released,  the  helper  T  cell  is  activated   • Activated  helper  T  cells  activate  CD8  (cytotoxic)  T  cells  and  B  cells   • B  cells  are  released  as  a  result  and  attach  to  the  foreign  antigens  directly     • CD8  cells  are  recruited  to  kill  the  exogenously  infected  cells  (Class  II  MHC)   • Overall:  Helper  T  cells  (CD4)  link  the  B  and  cytotoxic  (CD8)  T  cell  sides  à   Regulatory  cells  that  regulate  the  activity  of  other  cells   Slide  54:  Types  of  T  Cells:  Suppressor  T  Cells   • One  T  cells  are  activated  à  Clonal  selection  and  clones  are  continued  to  be   produced  until  suppressor  T  cells  shut  them  off   • Cytokines  produced  by  costimulatory  signals  or  lysis  chemicals  produced   by  T  lymphocytes  activate  suppressor  T  cells  that  produce  other  chemicals   to  stop  clonal  selection  to  ultimately  stop  the  immune  response   • In  general:  Suppressor  T  cells  are  activated  by  chemicals  that  activated  the  T   cells  to  begin  with  or  the  chemicals  produced  by  T  cells  that  are  released  in   the  process  of  the  antigen  they  are  trying  to  kill   Slide  55:  Primary  Immune  Response  Summary       Slide  56:  Immune  Disorders   • Immunodeficiency:   -­‐ Any  condition  that  causes  the  immune  cells  to  behave  abnormally     -­‐ Could  be  insufficient  production  of  immune  cells     -­‐ Could  be  that  there  are  enough  immune  cells  that  aren’t  doing  their   proper  function   • Autoimmune  Diseases:   -­‐ When  the  immune  system  attacks  its  own  body  cells  (Can’t  distinguish   MHC  “self”  markers  vs.  the  antigen  markers)   • Hypersensitivities:   -­‐ When  the  immune  system  responds  to  stimuli  that  wouldn’t  normally   activate  the  immune  system  (Harmless  cells  that  are  antigenic)   -­‐ Ex:  Allergies  caused  by  allergens  (antigens)   Slide  57:  Immunodeficiencies   • Congenital  Immunodeficiency:     -­‐ Genetic,  inborn,  from  birth   -­‐ Ex:  SCIDS  (Severe  Combined  Immunodeficiency  Syndrome)  à  Fails  to   produce  enough  T  and  B  lymphocytes  so  that  even  the  smallest  infection   can  be  detrimental   Slide  58:  Immunodeficiencies   • Acquired:   -­‐ Ex:  AIDS  (Acquired  Immunodeficiency  Sydrome)  à  HIV  virus  causes   AIDS  by  destroying  helpter  T  cells     o It’s  subsequent  infection  that  kills  a  person  with  HIV  since  there   are  no  helper  T  cells  available  to  get  rid  of  the  infection   Slide  59:  Autoimmune  Diseases   • Multiple  Sclerosis:   -­‐ Destroys  the  myelin  of  the  white  matter  in  the  brain  and  spinal  cord   -­‐ Lose  conductivity  and  can’t  send  electrical  signals  à  Loss  in  muscle   control  and  movement   Slide  60:  Autoimmune  Diseases   • Myasthenia  Gravis:   -­‐ Immune  cells  attack  neuromuscular  junction  in  skeletal  muscle     -­‐ Impairs  communication  between  nerves  and  skeletal  muscles   -­‐ Ex:  Loss  of  control  of  eye  muscles  as  seen  in  picture   Slide  61:  Autoimmune  Diseases   • Grave’s  Disease:   -­‐ Immune  system  attacks  the  thyroid  gland  so  that  it  produces  excessive   amounts  of  thyroxine   -­‐ Bulging  eyeballs  is  one  symptom     Slide  62:  Autoimmune  Diseases   • Juvenile  Diabetes:   -­‐ Type  I  Diabetes   -­‐ Immune  system  attacks  the  pancreatic  cells  that  produce  insulin   -­‐ Results  in  insufficient  insulin  production     Slide  63:  Autoimmune  Diseases   • Lupus:   -­‐ Immune  system  attacks  the  kidneys,  heart,  and  lungs   -­‐ Skin  lesions  association  to  where  someone  looks  like  they  have  been   bitten  by  a  dog  or  wolf   -­‐ Butterfly  rash  =  distinguishing  characteristic   Slide  64:  Autoimmune  Diseases   • Rheumatoid  arthritis:   -­‐ Immune  cells  attack  the  synovial  membranes   -­‐ Joints  destroyed  à  rheumatoid  arthritis     Slide  65:  Hypersensitivities:  Immediate     • Immediate  (Acute)  à  Anaphylaxis   -­‐ Response  to  allergen  occurs  within  contact   • Anaphylaxis:     -­‐ Systemic  release  of  histamine  that  causes  systemic  vasodilation  à   incredible  drop  in  blood  pressure     -­‐ Often  fatal   • EpiPen:   -­‐ Someone  is  told  to  carry  this  after  there  has  been  a  warning  in  an  initial   episode  where  the  person’s  body  responds  to  something  and  loses  the   ability  to  breathe,  drop  in  blood  pressure,  etc.   -­‐ Epinephrine  is  contained  in  the  EpiPen  and  causes  vasoconstriction  so   the  vasodilation  is  reversed  temporarily  (Must  get  to  the  hospital  still  as   soon  as  possible)   Slide  66:  Hypersensitivities:  Subacute   • Subacute:   -­‐ Response  to  an  allergen  occurs  a  few  hours  after  the  initial  contact   • Transfusion  reaction:   -­‐ When  the  wrong  blood  type  is  injected  in  another  individuals  body  à  The   body  starts  to  reject  the  blood   Slide  67:  Hypersensitivities:  Delayed   • Delayed:   -­‐ Response  occurs  1-­‐3  days  after  contact  with  the  allergen   • Poison  ivy  reaction     Slide  68:  Transplants   • Autograft:   -­‐ Transplant  from  one  part  to  another  part  of  the  same  body   -­‐ Only  works  in  some  cases   -­‐ Transplant  won’t  be  rejected   • Isograft:   -­‐ Transplant  from  an  identical  twin  since  twins  have  identical  MHC   markers  on  body  cells   -­‐ Transplant  won’t  be  rejected   • Allograft:   -­‐ Key  to  look  for  closeness  in  relatedness  in  relatives  (Can  include   strangers  though  too)   -­‐ The  closer  the  MHC  markers  on  body  cells  are,  the  less  likely  of  a  rejection   -­‐ There  is  still  possibility  of  a  rejection  due  to  donor  cells  being  foreign   cells  to  acceptor     • Xenograft:   -­‐ Transplant  from  a  different  species   -­‐ Ex:  Pig  heart  valves      


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