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Immunology > Humoral Immunity > Flashcards

Humoral Immunity Flashcards

1
Q

What two properties of antibodies are determining factors for effector function?

A

Heavy chain isotope switching (C region) and affinity maturation to enhance function

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2
Q

What are the effector functions of IgG?

A

Neutralization of microbes and toxins, opsonization for phagocytosis, activation of classical complement pathway, ADCC, neonatal immunity, feedback inhibition of B cell activation (Fc receptor)

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3
Q

What is the effector function of IgM?

A

Classical complement pathway activation

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4
Q

What is the effector function of IgA?

A

Mucosal immunity

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5
Q

What are the effector functions of IgE?

A

Defense against helminths and mast cell degranulation

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6
Q

What receptor extends the half life of IgG?

A

Neonatal Fc Receptor

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7
Q

How does the neonatal Fc receptor extend the half-life of IgG?

A
  1. Soluble IgG is phagocytosed into the endosome.
  2. IgG binds the Fc receptor in the endosome and is sorted to the recycling endosome instead of being degraded.
  3. At the plasma membrane, FcRn lets go of IgG at physiologic pH
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8
Q

Where is the neonatal Fc receptor expressed?

A

Placenta (important for passive immunity), endothelium, and phagocytes

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9
Q

How does IgG neutralize toxins and microbes?

A

Binds microbes or toxins and keeps from binding receptors or crossing epithelium. Most effective vaccines work via this method (diphtheria toxin)

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10
Q

What type of microbes are killed by opsonization and phagocytosis by IgG?

A

Encapsulated bacteria

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11
Q

What are the steps to opsonization and phagocytosis?

A
  1. IgG coats microbe
  2. IgG with microbe (IgG1 or IgG3): IgG Fc region binds high-affinity Fc receptors (FCgammaR1) on phagocytes. (requires >1 Ab binding)
  3. Fc receptor signal activates phagocyte and microbe ingested.
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12
Q

What type of infections are patients who undergo splenectomy susceptible to?

A

Infections by encapsulated bacteria because spleen is a major site for opsonization

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13
Q

Describe the affinity for IgG, where it is found, and the function of the FCgammaR1 receptor

A

High affinity for IgG
Found on macrophages, neutrophils, and eosinophils.
Function= phagocytosis

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14
Q

Describe the affinity for IgG, where it is found, and the function of the FCgamma RIIA receptor

A

Low affinity for IgG
Found in macrophages, neutrophils, eosinophils, and platelets
Function= phagocytosis

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15
Q

Describe the affinity for IgG, where it is found, and the function of the FCgamma RIIB receptor

A

Low affinity for IgG
B lymphocytes, dendritic cells, and mast cells
Feedback inhibition****

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16
Q

Describe the affinity for IgG, where it is found, and the function of the FCgammaRIIIA (CD16) receptor

A

Low affinity for IgG
Natural killer cells**
Antibody-dependent cellular cytotoxicity**

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17
Q

Describe the affinity for IgG, where it is found, and the function of the FCEpsilon R1 receptor

A

High affinity for IgE**
Mast cells, basophils, eosinophils
Degranulation of mast cells and basophils

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18
Q

What is antibody dependent cellular cytotoxicity and what Fc receptor is used?

A

Natural killer cells express FC gamma RIIIA and bind IgG stuck to antigen coated cells. Can also be used for tumor cells

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19
Q

Describe mast-cell mediated reactions with IgE

A
  1. IgE binds helminth
  2. IgE binds to FCEpsilonR1 receptor on eosinophils and receives IL-5 from TH2 cells
  3. Both receptor binding and IL-5 cause activation of eosinophils, degranulation, and release of toxic mediators
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20
Q

How is the alternative complement pathway activated?

A

C3 spontaneously activates to C3b

**Does NOT require antibodies

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21
Q

What happens after C3b binds the microbe plasma membrane in the alternative complement system?

A

C3a is released and Bb binds to C3b to form C3 convertase

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22
Q

What is the function of C3 convertase?

A

Cleavage of C3 into C3b and C3a

23
Q

How is the C5 convertase complex formed in the alternative pathway?

A

C3b binds the C3 convertase complex.

24
Q

What is the function of C5 convertase?

A

Massive cleavage of C5 into C5b and C5a

25
Q

How is the classical complement system initiated?

A

C1qr2s2 binds Fc on IgG on microbe PM

26
Q

What happens after C1 binds the Fc receptor on IgG in the classical complement system?

A

C1 undergoes conformational change to activate the r&s serine proteases

27
Q

What do the r&s serine proteases do in the classical complement pathway?

A

Cleave C4 and C2 into C4b and C2a

28
Q

What molecules make up the C3 convertase in the classical complement pathway?

A

C4b and C2a

29
Q

How is the lectin complement system pathway initiated?

A

Mannose binding lectin binds terminal mannose residues of microbial carbohydrates

30
Q

What happens after MBL binds the microbe in the lectin complement system?

A

MBL associated protease cleaves C4 into C4b and C2 into C2a

31
Q

What are the functions of C3 in the alternative pathway?

A

Opsonin and component of C3/C5 convertase. C3a stimulates inflammation

32
Q

What is the function of factor B in the alternative complement pathway?

A

Serine protease that is the active component of C3/C5 convertase

33
Q

What is the function of factor D in the alternative complement pathway?

A

Serine protease that cleaves factor B bound to C3b to activate it

34
Q

What is the function of properdin in the alternative complement pathway?

A

Stabilizes C3 convertase

35
Q

What is the function of C1 in the classical complement pathway?

A

binds Fc on Ab. R&S components cleave C4 and C2

36
Q

What is the function of C4 in the classical and lectin complement pathways?

A

C4b binds microbe surface and binds C2 for its cleavage by C1 or MBL protease.
C4a stimulates inflammation

37
Q

What is the function of C2 in the classical and lectin complement pathways?

A

Serine protease for active C3/C5 convertase

38
Q

How is the membrane attack complex formed and what is its function?

A

C5b is bound by C6, C7, C8, and C9.

C9 polymerizes to form a pore so water and ions can enter to lyse the cell

39
Q

What are the three functions of the complement system?

A
  1. opsonization and phagocytosis (via C3b binding microbe and being recognized by C3b receptor on phagocytes)
  2. complement-mediated cytolysis
  3. Stimulation of inflammatory reaction
40
Q

What three complement proteins formed in the complement pathways stimulate inflammation?

A

C5a, C3a, C4a (in order of potency)

Recruit leukocytes

41
Q

How do DAF and C1 inhibit the alternative and classical complement pathways?

A

Interfere with C3 convertase formation by either displacing Bb or C4b

42
Q

What is the function of MCP?

A

Cofactor for factor 1 cleavage of C3b to inhibit it.

43
Q

What is the role of C1-INH in the classical pathway?

A

C1 inhibitor that inhibits the C1 complex and can bind the MBL to inhibit the lectin pathway

44
Q

What is the role of CD59 in the complement system?

A

blocks C9 binding and prevents MAC formation

45
Q

What diseases are associated with deficiencies in C1, C2, C4?

A

Increased recurrence of infections and susceptibility to lupus

46
Q

Are C3 deficiencies common clinically?

A

No, C3 deficiency is usually fatal

47
Q

A deficiency in C9/ MAC formation is associated with what disease?

A

Nisseria infections

48
Q

Describe the pathology of paroxysmal nocturnal hemoglobinuria

A

RBCs lack DAF/CD59 complement inhibitors. RBCs are susceptible to MAC attack and lysing.

49
Q

What is one treatment for paroxysmal nocturnal hemoglobinuria?

A

Eculizumab anti-C5 antibody

50
Q

A defect in what component of the complement system is associated with hereditary angioedema?

A

Lack of C1-inhibitor. C1-inhibitor also functions to inhibit the cleavage and activation of kallikrenin. Active kallikrenin= bradykinin release. NOT a complement-mediated disease

51
Q

Heterozygous mutations in what genes are associated with atypical hemolytic uremic syndrome?

A 
MCP (cofactor for C3b cleavage/ inactivation)
Factor H (binds C3b to prevent Bb binding)
Factor I (cleaves C3b and C4b to inactivate)
52
Q

Describe the pathology and treatment for atypical hemolytic uremic syndrome

A

Small clots form in blood vessels (systemic thrombotic microaniopathy)
Treat with Eculizumab

53
Q

What is the CH50 test?

A

Measurement of classical complement pathway efficiency by measuring amount of RBC lysis. Result= amount of serum for 50% RBC lysis

54
Q

What are three ways pathogens have evolved to evade the humoral immune system?

A
  1. Antigenic variation (switch up Ags: HIV/ flu)
  2. Inhibition of complement activation
  3. Resistance to phagocytosis (pneumococcus)

Immunology (6 decks)

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