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Chapter 9 Immunity Mediated by  B Cells and Antibodies
Focus of Chapter 9  How Antibodies Clear Infection ,[object Object],[object Object],[object Object]
RECALL Pathogens extracellular Antibodies secreted in 2 ND  LT & Bone Marrow B cell function extracellular spaces Other Pathogens fluids B cell PM cell virus ~~~~~~ ~~~ Next cell bacteria Y Y Y intracellular virus
Ab    toxic    destructive to pathogens ,[object Object],[object Object],Molecular adaptor (opsonize) PHAGOCYTOSIS Neutralize = pathogen surface covered Growth/replication  Y 2 pathogen Y Y Y Y Y phagocyte ? ? 3 Role of AB = Y    reduces  infection Y Y Y 1 Y Y Y Y pathogen Y Y Y Y
COMPLEMENT activation ,[object Object],[object Object],[object Object],Complement = set of proteins that do not discriminate  between Ags 3
Antibody production by B lymphocytes
The Development Of B Cells Can Be Divided Into six Broad Phases
[object Object],[object Object],[object Object],[object Object],Peripheral circulation Bone Marrow
B cells need activated T cell help to mature into Ab-secreting Plasma Cells ,[object Object],[object Object],[object Object]
Last Two Main Phases of B-cell Development ,[object Object],[object Object],[object Object],[object Object]
T cell help, Isotype Switching  & Affinity Maturation  ,[object Object],[object Object],[object Object],[object Object],[object Object]
B cell Activation without T-cell Help ,[object Object],[object Object],[object Object],[object Object],[object Object]
7-1 B-cell activation requires cross-linking of surface immunoglobulin
Protein or carbohydrate epitopes Bacterial cell Naïve Mature B cell IgM’s    X-linked by repetitive Ag epitopes Ig    Ig  IgM  Ig    Ig  Note that BCR signal transduction resembles that of TCR Signal transduction extracellular   intracellular
How does BCR signal transduction resemble TCR  signal transduction ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],Similar intracellular signaling pathways!
B cell  Signal  Cascade ,[object Object],[object Object],[object Object],Tyrosine kinases Ig   cytoplasmic tail (mature naïve B cell) ITAMs phosphate Lyn
mature naïve Ig  Lyn ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],Transphosphorylation
What is the function of the previous intracellular pathway? ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
NO! Additional signals are required to “activate” a mature naïve B cell ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
How are signals delivered? ,[object Object],[object Object],[object Object]
Synergetic cooperation between B-cell receptor & B-cell co-receptor ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],Signal 2 Signal 1 Ig  Ig  : Lyn
Additional signals from  helper T cells are required ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
[object Object]
The Ab response to certain Ags  DOES NOT require T cell Help ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Whether a B cell needs T-cell help or not depends on the nature of the Ag ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
What is LPS? ,[object Object],[object Object],[object Object],[object Object]
LPS of gram-negative bacteria can activate B cells to become Ab-producing plasma cells ,[object Object],[object Object],[object Object]
LPS of gram-negative bacteria can activate B cells to become Ab-producing plasma cells ,[object Object],[object Object],[object Object]
There is a second type of TI Ag: TI-2 ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Ab responses induced by TI-2 Ags ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
9-4:  Activation of naïve B cells by most antigens requires help from CD4 T cells
B cells needing T-cell help  and Thymus-dependent Ags (TD Ags) ,[object Object],[object Object],[object Object],[object Object],[object Object]
B-cell Meets it’s Antigen ,[object Object],[object Object],[object Object],[object Object]
Mature naïve B cells need T-cell help with Thymus-dependent Ags (TD Ags) Ag delivery dendritic cells ,[object Object],[object Object],[object Object],CCL19 and 21 CCL13 ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],Infected tissue 
Mature naïve B cells become trapped in the T-cell zone of 2nd LT if they encounter their “cognate” helper T cell ,[object Object],[object Object],[object Object],[object Object],[object Object]
Does the BCR have a role  in B cell activation? ,[object Object],[object Object],[object Object],[object Object]
Two signals    B cell proliferation & differentiation into plasma cell B-cell activation in response to TD-Ag requires T cell help
What happens when TH2 cell’s TCR binds peptide Ag:MHC class II molecules on the B cell surface? ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
 
What happens to these dividing B cells? ,[object Object],[object Object],[object Object],A few days
How long does it take for a GC to appear? What is the physiological symptom of GC formation? ,[object Object],[object Object],[object Object],[object Object],[object Object],Medullary cords  PM cells IL5 & IL6 TH2 Y Y Y IgM 1° focus     1°   follicles Still attached to TH2 1 2 Can isotype switching happen in a primary follicle? Several days 1 week Lymph node swelling some Primary Focus B cells
Germinal Center ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
9-7 Activated B cells undergo somatic hypermutation and isotype switching in the specialized microenvironment of the B-cell zone
Common theme of lymphocyte development B cell maturation in germinal center Activation proliferation selection Activation proliferation selection
Proliferation in the GC, Okay What about hypermutation and affinity maturation in the GC? centroblasts dividing  in germinal center somatic  hypermutation & isotype switching T-cell cytokines Nondividing centrocytes Mutated surface Ig Post hypermutation Surface Ig of centrocyte Affinity for a specific antigen higher lower equal
What’s the upshot of this hypermutation & affinity maturation ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Mutated centrocytes compete! To engage a helper T cell Centrocyte    bind Ag    process antigen    surface = MHCII + Ag   Mutated centrocytes now compete! Access of Ag on FDC’s Ag-specific helper T cells MHCII 1 2 Follicular dendritic cells provide a source of intact Ag Mutated centrocyte
B cells recognize Ag as FDC surface “immune complexes” ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Iccosomes are  immune-complex coated bodies ,[object Object],[object Object],[object Object],[object Object],Iccosomes    taken up by Ag specific B cells in the GC    bound    B cells process & present Ag
Newly formed centrocytes move from the dark zone of the gc  to contact FDCs in the light zone ,[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object],[object Object]
Survivors interact with Ag-specific  T cells…Why? ,[object Object],[object Object],[object Object],[object Object]
What happens to centrocytes that fail to obtain, internalize & present Ag? ,[object Object],[object Object],[object Object],[object Object],[object Object]
Chapter 9 – Lecture Notes Immunity Mediated by  B Cells and Antibodies
Chapter 9 continued
9-9:  Interactions with T cells are required for isotype switching in B cells
Interactions with T cells are required for isotype switching in B cells, Why? ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
… Cognate interactions with helper T cell ,[object Object],[object Object],[object Object],[object Object],[object Object]
Interactions with T cells are required for isotype switching in B cells ,[object Object],[object Object],[object Object]
Which cytokines are most involved? ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
How do T-cell cytokines  induce isotype switching? ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
What else does isotype switching by cognate helper T cells require? ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Hyper-IgM syndrome No GC in Lymph Nodes  GC in Lymph nodes
Isotype switched, affinity matured B-cells can differentiate into plasma cells or memory cells ,[object Object],[object Object]
 
Antibody effector functions ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
9-11 IgM, IgG and IgA Abs protect the blood and extracellular fluids
IgM, IgG and IgA Ab functions ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Which blood-borne Ab is dominant  later in an immune response? ,[object Object],[object Object],[object Object],[object Object]
What about IgA? ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
IgA & IgG are transported across  epithelial barriers by specific receptor proteins ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
How are  IgA  & IgG  transported across epithelial barriers? ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
How are  IgA  & IgG  transported across epithelial barriers? Apical surface Basolateral surface Receptor mediated endocytosis Transcytosis
Brambell receptor (FcRB) ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Brambell receptor (FcRB)
Passive transfer of immunity ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
What about IgG during pregnancy? ,[object Object],[object Object],[object Object],[object Object]
Antibody production is  deficient in very young infants ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
High-Affinity IgG and IgA are used to  neutralize  microbial toxins and animal venoms ,[object Object],[object Object],[object Object],[object Object],[object Object]
High-affinity neutralizing Ab’s prevent viruses and bacteria from infecting cells
Ab’s link effector cells to the antigen ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Fc receptors ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Fc of Ab and Fc   receptor of effector cell
IgE binds to high-affinity Fc receptors on mast cells, basophils and activated eosinophils. ,[object Object],[object Object]
High points of 9.11 - 9.16 & 9.21 - 9.25 ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Immune complexes  and the complement system ,[object Object],[object Object],[object Object],[object Object]
Immune Complex Clearance ,[object Object]
 
Classical Complement Cascade ,[object Object],[object Object],[object Object],[object Object]
The complement system –  A review of what you have already learned. Slides 91 – 119 are to help you in remembering complement ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Complement components  circulate in blood and body tissues ,[object Object],[object Object],[object Object],[object Object],[object Object]
Complement components C3b and C3a  ,[object Object],[object Object],[object Object],[object Object],[object Object]
 
Several complement pathways ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Cascade ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
C3 ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
The complement component C1
 
Cleavage of  C4  exposes a  reactive thioester bond  that  covalently attaches  the  C4b fragment  to the  pathogen  surface
Activated C1s cleaves C4 and C2 to produce C4b and C2a, which associate to form the  classical C3 Convertase
Formation of the  alternative C3 convertase
The  two types of C3 convertase   have similar structures and functions
C3 activation by the alternative C3 convertase is a process analogous to C3 activation by the classical C3 convertase
View from above of complement deposition ,[object Object]
Cytolysis ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Inflammation ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
The Classical Pathway- Step 1: C1 component ,[object Object],[object Object],[object Object],[object Object],[object Object]
The Classical Pathway- Step 1: Activation of C1 ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
The Classical Pathway- Step 2: Activation of C4 ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
The Classical Pathway- Step 3: Activation of C2 ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
The Classical Pathway- Step 4: Cleaving C3 and amplification ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
The Classical Pathway- Step 4: Activation of C3 ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Wait a minute…What about MAC? ,[object Object],[object Object],[object Object],[object Object],[object Object]
The Classical Pathway- Step 5: Activation of C5, C6 and C7 ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
The Classical Pathway- Step 6: Activation of C8 and C9 ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
MAC
 
Complement System = Major defense mechanism against microbial infection ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]

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Immunology Chapter 9

  • 1. Chapter 9 Immunity Mediated by B Cells and Antibodies
  • 2.
  • 3. RECALL Pathogens extracellular Antibodies secreted in 2 ND LT & Bone Marrow B cell function extracellular spaces Other Pathogens fluids B cell PM cell virus ~~~~~~ ~~~ Next cell bacteria Y Y Y intracellular virus
  • 4.
  • 5.
  • 6. Antibody production by B lymphocytes
  • 7. The Development Of B Cells Can Be Divided Into six Broad Phases
  • 8.
  • 9.
  • 10.
  • 11.
  • 12.
  • 13. 7-1 B-cell activation requires cross-linking of surface immunoglobulin
  • 14. Protein or carbohydrate epitopes Bacterial cell Naïve Mature B cell IgM’s  X-linked by repetitive Ag epitopes Ig  Ig  IgM Ig  Ig  Note that BCR signal transduction resembles that of TCR Signal transduction extracellular  intracellular
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  • 30.
  • 31. 9-4: Activation of naïve B cells by most antigens requires help from CD4 T cells
  • 32.
  • 33.
  • 34.
  • 35.
  • 36.
  • 37. Two signals  B cell proliferation & differentiation into plasma cell B-cell activation in response to TD-Ag requires T cell help
  • 38.
  • 39.  
  • 40.
  • 41.
  • 42.
  • 43. 9-7 Activated B cells undergo somatic hypermutation and isotype switching in the specialized microenvironment of the B-cell zone
  • 44. Common theme of lymphocyte development B cell maturation in germinal center Activation proliferation selection Activation proliferation selection
  • 45. Proliferation in the GC, Okay What about hypermutation and affinity maturation in the GC? centroblasts dividing in germinal center somatic hypermutation & isotype switching T-cell cytokines Nondividing centrocytes Mutated surface Ig Post hypermutation Surface Ig of centrocyte Affinity for a specific antigen higher lower equal
  • 46.
  • 47. Mutated centrocytes compete! To engage a helper T cell Centrocyte  bind Ag  process antigen  surface = MHCII + Ag Mutated centrocytes now compete! Access of Ag on FDC’s Ag-specific helper T cells MHCII 1 2 Follicular dendritic cells provide a source of intact Ag Mutated centrocyte
  • 48.
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  • 55. Chapter 9 – Lecture Notes Immunity Mediated by B Cells and Antibodies
  • 57. 9-9: Interactions with T cells are required for isotype switching in B cells
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  • 63.
  • 64. Hyper-IgM syndrome No GC in Lymph Nodes GC in Lymph nodes
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  • 66.  
  • 67.
  • 68. 9-11 IgM, IgG and IgA Abs protect the blood and extracellular fluids
  • 69.
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  • 73.
  • 74. How are IgA & IgG transported across epithelial barriers? Apical surface Basolateral surface Receptor mediated endocytosis Transcytosis
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  • 80.
  • 81. High-affinity neutralizing Ab’s prevent viruses and bacteria from infecting cells
  • 82.
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  • 84. Fc of Ab and Fc  receptor of effector cell
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  • 95.
  • 96.
  • 97.
  • 99.  
  • 100. Cleavage of C4 exposes a reactive thioester bond that covalently attaches the C4b fragment to the pathogen surface
  • 101. Activated C1s cleaves C4 and C2 to produce C4b and C2a, which associate to form the classical C3 Convertase
  • 102. Formation of the alternative C3 convertase
  • 103. The two types of C3 convertase have similar structures and functions
  • 104. C3 activation by the alternative C3 convertase is a process analogous to C3 activation by the classical C3 convertase
  • 105.
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  • 117. MAC
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