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Immunology > 9 - Adapt 3: T Cell Activation > Flashcards

9 - Adapt 3: T Cell Activation Flashcards

1
Q

CD4 cells are:

A

T helper cells

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2
Q

what are the four main Th cells?

A

Th1
Th2
Th17
Treg

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3
Q

what stimulates differentiation into Th1

A

IL-12 and IFN-y

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4
Q

what stimulates Th2

A

IL-4

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5
Q

what stimulates Th17

A

TGF-B, IL-6, IL-21, IL-1B, and IL-23

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6
Q

where do the cytokines that stimulate differentiation come from

A

APCs

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7
Q

what stimulates Treg

A

TGF-B and Foxp3

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8
Q

what is Th1 involved in

A

cell-mediated immunity (intracellular bacteria and virus, autoimmunity)

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9
Q

what is Th2 involved in

A

humoral immunity (extracellular parasites, allergy, asthma)

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10
Q

what is Th17 involved in

A

cell-mediated inflammation, autoimmune diseases (extracellular pathogens and fungi, autoimmunity). Mainly neutrophils

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11
Q

what is Treg involved in

A

immunoregulation (switching off immune response)

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12
Q

what cell type does Th1 activate, and its effect

A

macrophages, via IFN-y, leading to cell mediated immunity

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13
Q

what cell type does Th2 activate and its effect

A

B cells, via IL-4, leading to class switching to neutralize antibodies and IgE

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14
Q

what cell type does Th17 activate and its effect

A

Neutrophils, via IL-17, to increase acute inflammation

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15
Q

bacteria + partial activation of macrophage with IFN-y =

A

granulomas in bovine tuberculosis

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16
Q

what is the pathogenesis of Th2 in response to parasites

A

parasites -> Th2 response -> IL-4, IL-5 and IL-13 -> decrease in parasites from direct killing (from class switching)

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17
Q

what is class switching?

A

idk I’ll fill this in later

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18
Q

pathogenesis of Th17 for extracellular pathogens

A

Th17 cells > Th17 cytokines >the
production of pro-inflammatory
cytokines > increase acute
inflammation through the recruitment of
innate immune cells such as neutrophils
> also promote further Th17 activation
in a positive feedback manner >
autoimmune diseases

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19
Q

T/F Treg subtypes activate Th1, Th2 and Th17

A

false, they suppress it

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20
Q

What causes feline immunodeficiency?

A

FIV activates Treg cells and replicates within these cells, and the Tregs become a virus reservoir for FIV, improving the viral survival and maintenance in the host. Therefore it is a lifelong disease

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21
Q

Porcine reproductive and respiratory syndrome virus (PRRSV) increase blood Tregs. T or F

A

true, leading to decreased immune response (because the Tregs are shutting it off)

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22
Q

Tregs in cattle in blood after BLV infection, T or F

A

true.

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23
Q

What are Memory T cells>

A

T cells that are first made in response to an antigen, that persist in the body so that a secondary antigenic response can be quicker and faster becuase the cells “remember” the antigen and can recognize is quickly

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24
Q

what happens during immunization

A

DCs take up antigens and present to naive T cells. Then the T cells are stimulated to proliferate and differentiate into effector and memory T cells

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25
Q

what are the three subsets of memory Tcells

A

central memory

Effector memory

Resident memory

26
Q

function of central memory (Tcm) cells

A

live longer, reside and travel between in
secondary lymphoid organs

27
Q

function of effector memory T cells (Te)

A

contribute better at first line of defense

28
Q

function of resident memory t cells (Trm)

A

permanent residents of previous infected tissues

29
Q

CD4 t cell memory

A

upon reinfection, CD4 memory cells can amount anamnestic responses that are quicker and of higher magnitude than a primary source

30
Q

CD8 T cell memory

A

5-10% of CTLs survive after primary infection to become memory CD8 T cells.

31
Q

Memory CD4 vs Memory CD8 T cells (NOT ON EXAM ACCORDING TO PROF)

A

Number of memory CD8T > memory CD4T cells
* Memory CD4 T cells proliferate > memory CD8T cells during secondary infection
* Memory CD8T cells more long lived than memory CD4T cells
* Following infection, memory CD4+ T cell help is necessary for the induction of a
memory CD8+ T cell pool
* Memory CD4+ T cell help promotes the induction of tissue-resident memory
CD8+ T cells during mucosal infection
* Regulatory T (T Reg) cells act during the resolution phase of infection to protect
CD8+ T cells from inflammatory signals and promote the survival of memory
CD8+ T cell pool

32
Q

when do memory T cells arise

A

within 3 days during the infection

33
Q

how are memory T cells maintained

A

IL-15 and IL-7 inputs allow for the maintenance of Memory T cells in the absence of the initial antigen

34
Q

what is the significance of IL-15 and IL-7

A

induce occasional division of memory T cells, which is involved in maintaining memory T cells without antigen input

35
Q

what are the three subsets of cytotoxic effector cells

A

CTLs, NK T cells, and NK cells

36
Q

what is the purpose of cytotoxic effector cells

A

eliminate infected cells and abnormal tumor cells (aka target cells)

37
Q

what are the two pathways in which CTLs can kill targets

A
  1. perforin/granzyme pathway
  2. Fas (CD95) - FasL (CD95-L) pathway
38
Q

what are the granules released by CTLs

A

granzyme, perforin and serglycine

39
Q

describe the perforin/granzyme pathway

A

granzymes enter the cell via receptor-mediated endocytosis, and enter the cytoplasm after perforin makes holes in the cell wall (activates apoptotic pathways)

40
Q

What is critical in the perforin granzyme pathway

A

ability to bind to target cells proficiently

41
Q

what is important for receptor phosphorylation in the perforin granzyme pathway

A

LcK

42
Q

T/F co-stimulation/signal II is required in the perforin granzyme pathway

A

false. it is not always required

43
Q

steps of granzyme perforin pathway

A
  1. conjugate formation
  2. CTL cytoplasmic rearrangement
  3. CTL granule exocytosis
  4. Dissociation
  5. apoptosis of target, recycling of CTL
44
Q

Describe the Fas (CD95) - FasL (CD95L) pathway

A

Fas is bound to FasL, which initates a death signal leading to apoptosis (cute lil pathology reminder)

45
Q

How do NK cells recognize their targets

A

they recognize the absence of MHC I on their targets and KILL EM

46
Q

How do NK cells react to healthy cells

A

healthy cells have lots of MHC I, so they induce a STRONG INHIBITORY signal in the NK cells

47
Q

how do NK cells react to tumor cells or virally infected cells

A

tumor cells or virally infected cells often downregulate MHC I, so there will be REDUCED INHIBITION and the NK cells will kill em

48
Q

how do NK cells react to transformed or some infected cells>

A

transformed or infected cells sometimes increase the expression of molecules that are recognized by activating NK cell receptors (activating ligands). Thist results in STONG ACTIVATION THAT OVERRIDES INHIBITION and the NK cell will kill em

49
Q

how do NK cells induce apoptosis of their targets

A

very similar to CTL, use perforins/granzymes at the junction between the two cells

50
Q

when are NK cells recruited

A

earlier than CTLs because they are part of innate response (day 1 ish)

51
Q

What are NKT cells

A

cells that are neither NK cells or T cells, and bridge the innate/adaptive immune systems.

52
Q

do NKTs have a TCR

A

yes but it is invariant and recognizes glycolipids presented by CD1d

53
Q

TF: NKT cells only act as killer cells

A

false. they can act as helper cells by secreting cytokines

54
Q

TF: NKT cells can form memory cells

A

false

55
Q

NKT posses T cell surface proteins rather than NK surface proteins

A

false. they have NK surface proteins rather than T cell varieties

56
Q

NKT kill primarily via the __ pathway, but can also kill via the ___ pathway

A

Fas-FasL, perforin/granzyme

57
Q

NKT have both ___ and ____ cell types

A

CD4+ and CD4-

58
Q

what do both the fas-fasL pathways activate

A

Caspase-3, which induces apoptosis

59
Q

What is a clinical application of cell mediated killing?

A

Chimeric antigen receptors (CARs)

60
Q

describe CAR immunotherapy

A

CAR immunotherapy
> modifying a cancer patient’s
own NK or T cells to express CAR and
antigen-specific antibody that
target tumor antigen > re-infusing these modified NK or T
cells back into the patient >
attack and kill cells expressing
the target antigen

61
Q

what is CAR therapy being used for in vetmed

A

Canine and feline lymphoma

62
Q

There is a slide called “Functions of T helper cell subsets”. go review it cuties

A

did you review it? Did you? D i d y o u?

good job

Immunology (18 decks)

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