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Immunology Exam 2 > Lecture 16 > Flashcards

Lecture 16 Flashcards

1
Q

What is the vaccine Ag for Polio? What is the protective mechanism?

A

Oral attenuated poliovirus

Neutralization of virus by mucosal IgA antibody

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2
Q

What is the vaccine Ag for Tetanus, Diphtheria

? What is the protective mechanism?

A

Toxoids

Neutralization of toxin by systemic IgG Ab

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3
Q

What is the vaccine Ag for Hepatitis A or B

? What is the protective mechanism?

A

Recombinant viral envelop proteins

Neutralization of virus by mucosal IgA or systemic IgG Ab

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4
Q

What is the vaccine Ag for Pneumococcal Pneumonia, Haemophilis? What is the protective mechanism?

A

CONJUGATE VACCINES composed of bacterial capsular polysaccharide attached to a carrier protein

Opsonization/phagocytosis mediated by IgM and IgG Abs, directly or secondary to complement activation

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5
Q

What are the 5 Effector functions of humoral immunity? For the first 2 functions, name the 2 vaccine examples for each.

A

Neutralization toxins/microbes
Ex. In polio, tetanus, Hep A/B

Opsonize (“tag”) for phagocytosis
Ex. Pneumoccal and other conjugate vaccines

Sensitize for Ab-dependent cellular cytotoxicity

Allows for NK cells to ID and destroy

Activate the complement system

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6
Q

Effector function for humoral immunity is mediated by the ___ ____

A

Fc Portion

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7
Q

How does humoral immunity neutralize toxins? Give an example of a toxin that our humoral immunity neutralizes in this manner.

A

BLOCK the binding of microbes and toxins to cellular receptors

Can prevent the spread of microbes from infected to healthy cell

Neutralization of the Influenza Virus is an example of how our humoral immunity prevents its spread

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8
Q

How does the humoral immunity opsonize microbes for phagocytosis? What binds to the pathogen? Note which portion of the Ig binds to the which receptor on the phagocyte. When does this occur in the immune response?

A

IgG binds to the pathogen

Fc receptor of Ig binds to phagocyte FcyRI (CD64)

  • This is a high-affinity receptor
  • BECAUSE OF THIS- FcyRI only works early in immune responses

-Activates signals -> activate phagocyte to destroy microbes

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9
Q

What kind of affinity is FcyRIIB? When does it work in the immune response?

A

Low Affinity

Later in the immune response

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10
Q

For Fc receptors (FcR) overall, describe what happens when they are activated or inhibited and what Ig they will use.

A

Activating R works early in response (IgM)
Inhibiting R works later in response (IgG)

Note- All FcR’s are activating except for fcyRIIB

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11
Q

What does FcyRIIB dysfunction lead to?

A

FcyRIIB- dysfunction -> increased susceptibility to SLE

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12
Q

What 2 cells is FcEpsilonRI located? What does it bind to? What is it useful in? When this receptor binds, what does it release? What type of affinity does this receptor have? When does it work in the immune response?

A

Found on eosinophils and mast cells
-Bind IgE Fc portion

Useful in protection against helminths

When bound to Fc portion of IgE -> release cationic protein that is toxic to parasites

When IgE binds -> Will automatically release mast cells

This happens in immediate reactions- VERY HIGH AFFINITY

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13
Q

What does FcyRIII bind to? What cell is FcyRIII found on? what does this binding activate? Describe the affinity and when it works in the immune response.

A

Ig binds to microbe and Fc binds to FcyRIII on NK cell

Activates NK cells to kill Ab-coated cells
-Via perforin and granzymes

Low Affinity -> Works later in immune response

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14
Q

Describe the Alternative Pathway for the Complement System.

A 
Spontaneous hydrolysis of C3 -> C3b
C3b binds to microbe and binds factor B -> C3 Convertase (C3bBb)
C3 convertase breaks more C3 to C3b
C3b binds to microbe -> C5 convertase
C5 convertase cleaves C5 to C5a and C5b
C5b + C6 + C7 + C8 + C9= MAC
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15
Q

Describe the Classical Pathway for the Complement System.

A

C1 binds to IgG or IgM bound to Ag via Fc portion
-Specifically C1q
-C1r and C1s= proteases
C1s cleaves C4 to C4a and C4b and C1 into C2a and C2b
C4bC2a -> C3 convertase
Cleaves C3 into C3a and C3b
-C3b can become part of the C5 convertase or enter alternative pathway
C3b binds C3 convertase -> C5 convertase (C4bC2aC3b)
C5b + C6 + C7 + C8 + C9= MAC

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16
Q

Describe the 4 steps involved in the formation of the MAC.

A
  1. Upon C5 activation, resulting C5b molecules has the binding site for C6
  2. When C5b-C6 have formed, C3b serves as an initial tether to anchor the molecule in place
  3. When C7 binds, it forms a transient anchor due to its hydrophobic region (if C7 fails to interact with the membrane, the complex at this point will inactivate by self-aggregation or by the inhibitors DAF or CR1)
  4. When C8 binds, it is responsible for inserting more deeply in the membrane allowing for a more permanent attachment
17
Q

Describe Complement Receptor 1 (CR1). What 5 cells is it found on? Describe its affinity and what 2 molecules it binds. What are the 3 functions of CR1?

A

On phagocytes, neutrophils, B and T cells, erythrocytes

HIGH AFFINITY for C3b and C4b

Functions:

  • Promote phagocytosis of C3b and C4b coated particles
  • Clearance of immune complexes
  • Activates killing mechanisms of phagocytes
18
Q

Describe Complement Receptor 2 (CR2). What cell is it found on? Describe its affinity and what 2 molecules? What does it enhance? What type of infection is it associated with?

A

On B lymphocytes

HIGH affinity for cleavage products of C3b (C3d and iC3b)

Enhances response of B cell to Ag when bound

*Associated with Epstein Barr Viral infections

19
Q

Describe Complement Receptor 3 (CR3). What 3 cells is it found on? What 2 molecules does it bind and what does each induce?

A

On phagocytes, NK cells, Neutrophils
AKA Mac-1

Binds iC3b to induce phagocytosis

Can also bind ICAM-1 (necessary for the recruitment of leukocytes)

20
Q

Describe Complement Receptor 4 (CR4).

A

Pretty much the same as CR3 except that it only binds iC3b

21
Q

Describe each of the following complement regulators:
*Note the effects and which pathways it blocks

C1 Inhibitor

DAF

CR1

MCP

Factor I

CD59

A

C1 inhibitor- INHIBITS CLASSICAL ACTIVATION

DAF- Blocks C2:C4 interactions, dissociate C4bC2a OR C3bBb (INHIBITS classical or alternative)

CR1- dissociates C4bC2a OR C3bBb
-With FI, cleaves C4b or C3b, phagocytosis when bound to C3b (all pathways)

MCP- is a cofactor for Factor I

Factor I causes the conversion of C3b to iC3b (inactive form)

CD59- inhibits MAC formation by blocking the addition of C9

22
Q

What is the Complement Deficiency and its effect for the disease SLE?

A

C1q, C2, C4

Failure of clearing immune complexes.
Will be deposited on BV and lead to inflammation

23
Q

What is the Complement Deficiency and its effect for frequent pyogenic bacterial infections?

A

C3

Can be fatal.
Don’t have any complement essentially

24
Q

What is the Complement Deficiency and its effect for increased susceptibility to pyogenic bacteria?

A

Properdin and Factor D

Unstable C3 convertase in alternative complement pathway

25
Q

What is the Complement Deficiency and its effect for Neisseria Bacteria?

A

C5-C9

26
Q

What are the 3 pathologic effects of te complement?

A

Tissue damage with acute inflammation responses generated

Thrombosis

Nephropathy (MAC mediated)

27
Q

How do Sialic Acids evade the complement system? What complement regulatory protein does it recruit?

A

Inhibit alternative pathway

Recruit Factor H -> Removes C3b from Bb

28
Q

What 2 complement regulatory proteins does HIV produce to evade the complement system?

A

DAF and CD59

Immunology Exam 2 (10 decks)

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