Assignment 6 Flashcards

1
Q

what do NK cell arise from

A

bone marrow precursors (lymphoid progenitor cells)

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2
Q

where are NK cells found

A

blood, spleen, peritoneal exudate

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3
Q

role of NK during a CD4+ Thp cell activation

A

NK cell which is activated by IL-12 secretes IFNγ which influences the Th0 differentiation primarily to a Th1 subset

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4
Q

role of NK cells in viral infection and cancer

A

kill autologous cells that are virally infected or infected with cancer by releasing its granules perforin and granzyme and escaping the region so as not to be affected by the toxic effects of the released granules

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5
Q

what cytokine is released when NK cells are stimulated with IL-12

A

IFNγ

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6
Q

role of IL-15, and IL-18 when NK cells are stimulated with IL- 12

A

they enhance IFNγ induced by IL-12

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7
Q

source of IL-12, IL-15, IL-18

A

dendritic cells and macrophages

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8
Q

role that interferon gamma (IFNγ) plays in the differentiation of Th0 cells to CD4+ T cells

A

it influences Th0 differentiation primarily to a Th1 subset

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9
Q

how are lymphokine activated killer (LAK) cells generated and what is its unique property

A

in the presence of high concentration IL-2, NK cells differentiate to LAK cells which are potent killers of tumor cells

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10
Q

NK cells express activating and inhibitory receptors that interact DIRECTLY with ligands on the target cell. What are the three classes of ligands for these receptors?

A

specific self - Class I MHC
MHC Class-I like molecules
molecules unrelated to MHC

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11
Q

“stress- induced” ligand that allows NK cells to destroy target despite normal expression of Class I MHC

A

MICA (MHC Class I chain related gene A)

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12
Q

three conditions in which MICA is upregulated

A

on virally infected cells, cancer cells,

Stress :)

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13
Q

three conditions in which Class I MHC decreases on target cell

A

stress, some viral infections, some tumors

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14
Q

two cytokines whose interaction with target cells leads to upregulation of Class I MHC

A

IFNγ (Type 2 interferon) or IFNα/β (Type 1 interferons)

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15
Q

source of IFNγ, IFNα, IFNβ

A

IFNγ - CD4+ Th1 cells, NK cells
IFNα - virally infected leukocytes
IFNβ - virally infected fibroblasts

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16
Q

how does the balance of activating and inhibitory receptors on the NK cell determines the fate of the target cell

A

if the inhibitory receptor on NK cells is strong enough, the cell expressing Class I MHC is protected and the cell tolerance is maintained

if the activating receptor on NK cells is stronger, the cell will not be protected and will be destroyed

17
Q

why does NK cells not destroy host cells in the absence of infection or tumors

A

infections and tumors decrease the amount of self Class I MHC-self peptide expression which makes it impossible for NK inhibitory receptors to deliver inhibitory signals because of insufficient self Class I MHC-self peptide so activating receptor takes over and cell is destroyed

without infection and tumors, there is a sufficient amount of self Class I MHC-self peptide so inhibitory receptor can deliver its signal hence protecting the cell

18
Q

two molecules that are released from the granules extruded by NK cells (NK cell armamentarium)

A

granzymes

perforin

19
Q

immune processes that led to the binding of Fcγ to the target cell

A

it recognizes Fc region of antibodies so if there is an antibody present on a target cell then Fcγ will bind to it

20
Q

how are target cells killed when Fcγ binds to it

A

there is a release of perforin and granzymes which destroys the target cell

21
Q

why are NK cell not destroyed itself in the process of killing a target cell

A

granules polarize to the conjugation region and is released in a way that allows the NK cells to escape the harmful effects of granzymes and perforin

22
Q

why is the Fcγ-FcγR mode of recognition for target cell destruction referred to as “antibody-dependent cell mediated toxicity” (ADCC)

A

because different antibodies recognize different viral proteins embedded in the cell membrane of the infected cell and then kill the infected cell