3Aa. S3/b3 Humoral Effectors

Front 1

What is pyogenic bacteria?

Back 1

Bacteria that forms pus

Front 2

Is Humoral immunity targeting extracellular or intracellular?

Back 2

Extracellular

Front 3

What is humoral immunity mediated by?

Back 3

Antibodies using B-lymhocytes

Front 4

What are the two main functions of antibodies?

Back 4

1. Neutralize toxins and viruses
2. Opsonize bacteria

Front 5

What is opsonization?

Back 5

Identifying a bacteria for phagocytosis

Front 6

What are thymus dependent antigens made of versus thymus independent antigens?

Back 6

1. Proteins
2. Cross linking lipids and polysachs

Front 7

How does complement work in B-cell activation?(4) Tcell independent.

Back 7

2. C3d/microbe binds CR2 on B-cell
3. IgM also binds
4. Cr2/IgM complex signals B-cell activation

Front 8

How do B cells get activated by a thymus dependent antigen?(4)

Back 8

1. TH1 needs to recognize MHC2
2. B7/CD28 bind, then CD40/CD40L bind
3. Releases IL-4 and IL-5
4. B-cells activate and proliferate

Front 9

What does IL-4 do?(2)

Back 9

1. A b-cell growth factor
2. Also stimulates IgE

Front 10

What does IL-5 do?(3)

Back 10

1. B-cell differentiation
2. Also Eosinophils
3. IgA

Front 11

What happens to people with x-linked hyper IgM syndrome?(3)

Back 11

1. Mostly males
2. Recurrant resp infections
3. Deficient CD40L

Front 12

What is the variable Ig region?

Back 12

The heavy chain not the Ag binding site

Front 13

What is the structure of the Ig's?

Back 13

1. IgG, IgE = monomer
2. IgA = dimer
3. IgM = pentamer
4. All have 2 heavy and 2 light chains

Front 14

What parts of the chains are variable?

Back 14

The tips of the H and L chains in the Fab fragments

Front 15

The Fc and Fab regions are made of what?

Back 15

1. Fc = only heavy chains
2. Fab = both heavy and light chains

Front 16

What does the Fab region do?

Back 16

Only ab binding

Front 17

What does the Fc region do? 4 C's

Back 17

1. Carboxy terminus
2. Constant
3. Complement binding (IgM and IgG)
4. Carbohydrate side chains

Front 18

Ab Digestion seperates them into what three parts?

Back 18

1. Pepsin = Fab region
2. Papaom = 2Fab and Fc
3. Mecaptoethanol = Light and heavy chains

Front 19

What does IgG do?

Back 19

1. Activate complement
2. Opsonizes
3. Mediates ADCC

Front 20

What does IgD do?

Back 20

Nothing

Front 21

What does IgE do?(3)

Back 21

1. Mediates Type 1 hypersentivity
2. bound to mast cells/basophils(Fc-epsilon-R1-R)
3. Helmints

Front 22

What does IgA do?

Back 22

1. Breast milk Ab
2. Main Ig in secretions
3. Produced in Submucosa, prevents bacteria binding here

Front 23

What does IgM not do?

Back 23

1. Not an opsonin
2. Not mediate ADCC

Front 24

What is a J chain?

Back 24

It likes Ig multimers together

Front 25

What is the poly Ig receptor

Back 25

Responsible for pulling IgA into the mucosa for secretion

Front 26

Once the Ab docks at the Fc site on a mast cell what is needed for degranulation?

Back 26

Cross linking with another IgE

Front 27

How do ab neutralize toxins?

Back 27

1.They use the two chains to occupy the various binding sites
2. Then they can stick together and precipitate out of solution for phagocytosis
3. Or they can fix complement for lysis

Front 28

What does the TCR complex do?

Back 28

Recognizes peptide antigens and signals CD40L production

Front 29

Which IgG's are responsible for opsonizing microbes? What happens after that?

Back 29

1. IgG1 and IgG3
2. The Macrophages have Fc receptor sites and eat those microbes

Front 30

What does CD16(FcR3A) do? What does FcEpsilonR1 do?

Back 30

1. ADCC on NK cells
2. IgE and Mast cell degranulation

Front 31

Which Ig represents ADCC?

Back 31

1. IgG
2. Has FcR3A
3. Binds to NK cells for microbial lysis

Front 32

What is Valence? What is affinity? What is Avidity?

Back 32

1. The number of antigen binding sites
2. The strength at which ag binds ab only one
3. Multiple epitopes on Ag interact with multiple Ab binding sites = Depends on Valance and Affinity

Front 33

What are RAG-1 and RAG-2?

Back 33

Enzymes that recombine the H chain variable regions.

Front 34

What is AID?

Back 34

1. Activation induced cytidine deaminase
2. Critical enzyme in somatic hypermutation

Front 35

What is somatic hypermutation?

Back 35

1. CDR point mutations that change the affinity for Ag

Front 36

What is isotype switching?

Back 36

1. The changing of Ig's from default(IgM with no cytokines) to the others
2. IFN will make IgG1 or IgG3 for TH1
3. IL-4 will make IgE from TH2
4. TGF, APRIL and BAFF will make IgA

Front 37

What is C3b?

Back 37

1.The most important complement that opsonizes bacteria
2. binds to CCR1 receptors on phagocytes

Front 38

What does the MAC do?

Back 38

Creates pores in cell membranes and causes osmotic lysis

Front 39

What complements stimulate inflammation?

Back 39

1. C3a, 4a and 5a
2. Recognized by neutrophils

Front 40

What is C3 convertase? What do the cleavage parts do?

Back 40

1. Complex of C2a and C4b
2. Cleaves C3 into C3b
3. C3b goes on to opsonize bacteria
4. C3a acts as a chemoattractand

Front 41

What is BAFF?

Back 41

A b-cell activating cytokine

Front 42

What do C2 and C4 do?

Back 42

Important in clearing immune complexes

Front 43

How does the alternative pathway work?

Back 43

1. C3b lands on a microbe
2. Binds with Factor B
3. More C3 convertase makes more C3b
4. Now C5 convertase makes C5b
5. Late steps of activation

Front 44

How does the classical pathway of complement work?

Back 44

1. C1 binds Ag/Ab molecules
2. C3 and C5 convertases formed
3. Cleavage of C5 into C5b
4. Late steps of activation

Front 45

Describe the late steps of complement activation?

Back 45

1. Formation of the MAC
2. C5b binds C5 convertase
3. C6 and C7 and C8 are bound and inserted into lipid bilayer
4. 15 C9's attach to form MAC
5. Creates pores in the cell and osmotic lysis

Front 46

What is osmotic lysis an important defense against?

Back 46

Neiserria because it has thin walls

Front 47

How do they regulate complement? The major regulatory proteins?

Back 47

1. DAF or CR1 will prevent C3 convertase(alternative) or C4b(classical
2. Major proteins are FDCs and MAC

Front 48

What would a deficiency of C3 causes? C2 and C4? C9?

Back 48

1. Susceptibility to infections
2. Immune complex Dz = Type 3
3. Increased Neisseria infections

Front 49

Describe B-cell germination?

Back 49

1. Antigen activated B-cells undergo clonal expansion
2.Somatic Hypermutation
3.Centrocytes go to light zone
4. Reselection with T-cells and FDCs
5. Those selected will differentiate into plamsa(CSR) and memory B cells