chapter 12 Flashcards

1
Q

What are the 6 antibody-mediated effector functions?

A
  1. Neutralization
  2. Agglutination
  3. Opsonization
  4. Complement Activation
  5. Antibody-Dependent Cell-Mediated Cytotoxicity (ADCC)
  6. Antibody-Dependent Degranulation and Mediator Release
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2
Q

protects against viral or bacteria infection or the damaging effects of toxins

A

neutralization

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3
Q

enhances neutralization and more efficient clearance of pathogens form the body

A

agglutination

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4
Q

promotes and/or enhances the engulfment of antigens by phagocytes

A

opsonization

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5
Q

results in the generation of the membrane attack complex (MAC), creating pores in pathogen membranes and killing the microbe

A

complement activation

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6
Q

activates the killing activity of several types of cytotoxic cells, e.g., NK cells

A

antibody-dependent cell-mediated cytotoxicity (ADCC)

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7
Q

triggers mediator release from granulocytes

A

antibody-dependent degranulation and mediator release

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8
Q

Which immunoglobulin has the highest molecular weight?

A

IgM because it is a pentamer

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9
Q

Which antibody is the first produced in a primary response?

A

IgM

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10
Q

describe the effector functions of IgM:

A

-lower affinity
-pentavalent
-very good at complement fixation leading to MAC formation and target lysis
-efficient at forming dense Ab-pathogen complexes that are efficiently engulfed by macrophage

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11
Q

What are the subclasses of IgG and their distinct effector capability?

A

-Human IgG1/IgG3 effective at complement fixation
– Mouse IgG2a/human IgG1 good at mediating ADCC by NK cells

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12
Q

What is the major Ig isotype found in secretions like tears and mucus?

A

IgA

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13
Q

describe the effector functions of IgA:

A

-effective at neutralizing toxins and pathogens
-does not fix complement, so does not drive inflammation
-long half-life in secretions due to protease-resistant amino
acid sequence in Fc region

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14
Q

describe the effector functions of IgE:

A

-best known for role in allergy and asthma
-may also play a role in protection against parasitic helminths and protozoa
-degranulation of eosinophils/basophils
-release of molecules such as histamine to damage large pathogens

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15
Q

what are the 3 subsets of cytotoxic effector cells?

A

-cytotoxic T lymphocytes
-NK T cells
-NK cells
*these eliminate infected cells and abnormal tumor cells

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16
Q

CTLs recognize and kill infected/tumor cells via ___________________

A

TCR activation

17
Q

CTL signal 1:

A

TCR binds peptide presented by APC on MHC class I

18
Q

CTL signal 2:

A

-costimulatory signal transmitted by CD28-B7 (B7-1: CD80, B7-2: CD86) interaction between T cell and APC
– APCs get help from T cells to upregulate stimulation molecules

19
Q

CTL signal 3:

A

provided by IL-2, inducing proliferation and differentiation into CTL form

20
Q

-4 peptide-bound MHC I molecules bound together and conjugated to a fluorescence marker

A

MHC tetramers

21
Q

Describe how CTLs can be tracked with tetramers:

A

-tetramer recognizes CTLs with a TCR capable of binding peptide/tetramer
-flow cytometry is used to detect fluorescent cells
-very sensitive

22
Q

What are the two mechanisms for initiating CTL-mediated apoptotic death of target cells?

A
  1. Directional delivery of cytotoxic proteins (perforin and granzymes) that are released from CTLs and enter target cells.
  2. Interaction of the membrane-bound Fas ligand on CTLs with the Fas receptor on the surface of target cells.
23
Q

What is Fas-FasL mediated cytolysis?

A
  • FasL is found on CTLs
  • Fas is found on target cell
  • Fas bound by FasL initiates a death signal leading to apoptosis
24
Q

Natural killer cells make up 5-10% of what population?

A

circulating lymphocyte population

25
Q

-non-specific cytotoxicity
-the first line of defense against viral infection
-Kill virus and other intracellular pathogen-infected cells, and tumor
-Produce cytokines to regulate innate and adaptive immunity

A

natural killer cells

26
Q

How are NK cells different from CTLs?

A

– No Ag Specific TCR
– No MHC restriction
– No memory, same intensity regardless of repeated
exposure

27
Q

What are candidates for activating signals in the missing self model?

A

C-type lectins

28
Q

Describe the inhibitory receptors of the missing self model:

A

– CD94/NKG2 recognize HLA-E
* If HLA-E is present - inhibitory signal, no killing
* No HLA-E (during viral infection) - no inhibitory signal, killing
– KIRs recognize specific MHC molecules - inhibitory signal, no
killing

29
Q

Describe the entire process of the missing self model:

A

-Normal cells present a ligand for the activating (killing) receptor on NK cells AND an MHC class I ligand for the inhibitory receptor
-When viruses infect cells, some may inhibit MHC class I expression
to evade detection and elimination by CTLs
-The balance of inhibitory vs activating signals determines whether NK is
activated or not

30
Q

How do NK cells induce apoptosis of their targets?

A

Once activating signal molecules are engaged, NK cells use mechanisms very similar to CTLs to induce target cell death
– Release of perforins/granzymes at junction of two cells

31
Q

Describe the nature of NK cells:

A

-large granular lymphocytes
-lack T cell receptor, CD3 proteins, and surface IgM and IgD
-thymus not required for development
-normal numbers in SCID patients

32
Q

What are the many functions of NK cells?

A

-kill virus infected cells and cancer cells (nonspecific)
-killing is not dependent on foreign antigen presentation by Class I or II MHC proteins
-killing is activated by failure of a cell to present self antigen in association with Class I MHC proteins or by a reduction in the number of Class 1 MHC proteins on the cell surface
-kill by producing perforins and granzymes, which causes apoptosis of target cell

33
Q

NKT cells bridge ______________________immune systems.

A

innate/adaptive

34
Q

What does the TCR of NKT cells recognize?

A

glycolipids presented by nonpolymorphic CD1d

35
Q

Describe NKT cells:

A

Can act as helper cells (secreting cytokines) or killer cells
– Killing seems dependent on Fas-FasL interactions
* Include both CD4+ and CD4– cell types
* Don’t form memory cells
* Possess NK surface proteins rather than T-cell varieties