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MICR 386 > Module 7 > Flashcards

Module 7 Flashcards

Cell-Mediated Immunity

1
Q

sequence of cell mediated immunity (CMI)

A

effector cells are responsible for the immune response in CMI
- immune response can be divided into two phases based on the effector cells present: non-specific and specific

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2
Q

non-specific CMI

A

responses performed by macrophages and NK cells, which result in an increased IFN-a and IFN-b
- in the later stages of the non-specific stage of the response, continued contribution of macrophages will activate Th1

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3
Q

specific CMI

A

includes responses performed by cytotoxic T cells, which are activated by Th1 cells

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4
Q

antigen non-specific effector cells

A

these can recognize pathogens, but are not specific to a particular antigen
- they do not distinguish one pathogen from another

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5
Q

antigen specific effector cells

A

CTLs are effector cells specific for a processed pathogen antigen in complex with MHC class I

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6
Q

non-specific effector cells: macrophages

A

the initial macrophage response is nonspecific
during later stages, antigen specific Th1 cells play a role in activating the macrophage response

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7
Q

macrophage functions

A

produce reactive oxygen intermediates, nitric oxide and lysosomal enzymes
secrete cytokines
activate NK cells during infection

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8
Q

non-specific effector cells: NK cells

A

NK cells play a role in the early response to infection
- NK response can be activated by IFN-a, IFN-b, and IL-2

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9
Q

NK cell functions

A

Fas-mediated killing
control infection during the period required for generation of specific cells
involved in ADCC

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10
Q

specific effector cells: CD4+ Th1 cells

A

antigen specific effector T cells are specialized to deal with different classes of pathogens
- Th1 activates macrophages, NK cells, and CTLs

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11
Q

Th1 and Th2 cell actions

A

Th1: results in CMI response
Th2: results in humoral immune respones

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12
Q

specific effector cells in CMI: CD8+ CTL

A

antigen specific effector T cells are specialized to deal with different classes of pathogens
- CTLs kill pathogen infected cells

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13
Q

CTL antigen recognition

A

CTLs are CD8+ cells that kill target cells that display peptide fragments of cytosolic pathogens bound to MHC class I molecules (ex: kills influenza virus)

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14
Q

CD4+ antigen recognition

A

expressed by Th2 cells, recognizes fragments of antigens degraded within intracellular vesicles displayed by MHC Class II molecules (ex: kills M. tuberculosis)

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15
Q

Th1 cell function vs CTL cell function

A

Th1 cells activate macrophages, NK cells, and CTLs, enabling them to destroy pathogens efficiently
CTLS kill infected target cells

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16
Q

clinical applications of CMI effector cellls

A

delayed type hypersensitivity (DTH) is a response mediated by sensitized helper T cells, which release various cytokines. DTH plays a part in macrophage clearance and killing of intracellular pathogens. DTH is the result of cytokine release from CMI effector cells

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17
Q

DTH responses

A

DTH responses in the skin have been used to test CMI in vivo
- if testing for TB, a positive test requires a subject’s exposure to the antigen to be at least 4-6 weeks prior to skin testing. positive tests are seen as erythema and induration 48-72 hours post injection
- a 10 mm induration is considered positive, and indicates immune sensitization only

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18
Q

effector cells in DTH

A

cytokines released from activated helper T cells elicits a DTH reaction
- cytokines modulate expression of cell adhesion molecules and promote monocyte to macrophage differentiation in the tissue

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19
Q

effects of activated CMI effector cells

A
  1. cytokines: Th1 effector cells from previous immunization recognizes the antigen and releases cytokines
  2. recruitment: recruitment and activation of more T cells, neutrophils, and macrophages to the site of antigen injection
  3. inflammation: recruited cells cause inflammation to the area
20
Q

phagocytosis steps

A

attachment
ingestion
fusion
digestion
release

21
Q

effects of macrophages in CMI

A
  1. production of reactive oxygen intermediates, nitric oxide, and increased lysosomal enzymes: kills microbes in phagolysosomes
  2. secretion of cytokines: TNF, IL-2: recruits leukocytes for inflammation. IL-12: Th1 differentiation
  3. increased expression of B7 costimulators, MHC molecules: increased T cell activation
22
Q

effects of increased IL-12 secretion

A

IL-12 induces differentiation of naive CD4 Th0 cells into Th1 cells

23
Q

NK cells

A

activated by interferons and macrophage derives cytokines to serve as an early defence against certain intracellular infections

24
Q

NK cells target recognition recognition

A

killer inhibitory receptors (KIRs) are present on NK cells and recognize MHC class I
- all normal host cells/somatic cells express MHC class I molecules, therefore, when KIRs recognize these molecules, there is no killing of the normal cells
- virally infected cells have a downregulated expression of MHC class I molecules. In the absence of MHC class I molecules, KIRs are not engaged, ultimately resulting in signalling the NK cells to kill the cell

25
Q

antibody dependent cell mediated cytotoxicity (ADCC)

A

a mechanism by which NK cells interact and kill target cells
- steps include antibody opsonization, NK cell CD16, activated NK cell

26
Q

ADCC antibody opsonization

A

infected target cells express pathogen antigens on their cell surface
- these cells are recognized by specific antibodies produced by antibody secreting plasma cells
- this process is called opsonization

27
Q

ADCC: NK Cell-FcyRIII (CD16)

A

NK cells express CD16 receptors, which recognize and bind the Fc portion of antibodies
- once CD16 of an NK cell binds to an antibody attached to a target cell, NK cell is activated

28
Q

ADCC: activated NK cell

A

activated NK cells bound to a target cell release the content of their cytolytic granules by directly killing the target cell or by inducing Fas L/Fas-mediated apoptosis

29
Q

cytotoxic T lymphocytes (CTLs)

A

the process of antiviral T cell activation is delayed in the generation of antigen specific CTLs
- due to their specificity, CTLs mount a more effective and lasting response against the virally infected cell than the initial non-specific immune response by NK cells

30
Q

CTL activation

A

once immunocompetent naive CTLs are circulating in the organism, they require 3 signals to kill a target cell:
- adhesion
- antigen presentation
- activation

31
Q

CTL activation: adhesion

A

interactions of T-cells with their targets initially involves non-specific adhesion molecules
- the initial interaction is formed by integrin LFA-1 on the T cell, and ICAM-1 on their target cell

32
Q

CTL: antigen presentation

A

the interaction between adhesion molecules ensures that the T cell remains in contact with the target cell
- TCR peptide: MHC complex, in association with CD28 and B7, provides a signal to activate the CTL

33
Q

CTL: activation

A

poised or partially activated CTLs express high levels of the IL-2R beta chain and low levels of the IL-2R alpha chain
poised CTLs secrete small amounts of IL-2, but not enough for full activation of the CTL. Poised CTL requires additional IL-2 from CD4+ Th1 cells

34
Q

clonal expansion of CTLs

A

secretion of IL-2 from CD4+ helper Th1 cells increases p55-alpha expression for IL-2R, which permits the formation of high affinity IL-2R
- increased expression of IL-2R binds more IL-2 secreted from Th1 cells, allowing for clonal expansion of activated CTLs

35
Q

clonal expansion

A

responsible for the strength and specificity of the cell mediated immune response
- it results in an increased number of cytotoxic T cells that are specific for an processed antigen expressed on MHC class I that can travel throughout the body to fight infection

36
Q

MHC restriction of CTLs

A

during clonal expansion, activated CTLs develop:
- cytoplasmic granules that contain perforins, serine esterases, granzymes, toxins, etc.
- cytotoxic cytokines that induce IFN-y, TNF-b, which can inhibit viral replication and are involved in the activation and recruitment of macrophages

37
Q

MHC Class I restricted CTL

A

two responses can be elicited when CTLs interact with processed antigenic peptide presented by MHC on a target cell
- either no recognition, or peptide/MHC specific recognition

38
Q

no recognition

A

no recognition = no killing
if the TCR of a CTL does not recognize both the peptide and the MHC complex presented on a target cell, then the activated CTL will not recognize the antigen presenting target cell
- the CTL will separate from the target cell and not result in killing of the target cell

39
Q

peptide/MHC specific recognition

A

recognition = killing
when the peptide:MHC complex is recognized by TCR, a series of events will activate the CTL effector functions
- the effector CTL will kill the target cell

40
Q

polarization of T cells during killing steps

A
  1. TCR of the CTL recognizes peptide:MHC complex. The LFA-1 of the T cell adheres to ICAM-1 of the target cell
  2. TCR:MHC binding and adhesion molecules signals for the effector molecules in T cell to re-orient towards the target cell. effector molecules include MTOC, Golgi, and cytotoxic granules 3. re-orientation results in a lethal hit of cytotoxic granules to target cell at the point of contact (first punch) 4. cytotoxic granules release perforin in a directed fashion to target cell. at the site of cell-cell contact, perforins undergo Ca2+-dependent polymerization which forms pores in target cell membrane
  3. pores formed allow entry of granules (ex: granzymes) which initiates cell death by apoptosis
41
Q

membrane damage to target cells

A

results in a visible cavity, influx of water, and swelling of the target cell ultimately, killing the target cell

42
Q

T cell polarization

A

once the CTL is activated, it becomes polarized
- polarization of T cells results in conformational changes of the components of the T cell that promote pore formation in the target cell
- polarization of T cells leads to pore formation in the target cell

43
Q

what would happen with a perforin deficiency

A

FHL is a disease caused by perforin deficiency, meaning CTLs and NKs cannot create perforin
- as a result, the CTL stays intact and its ability to kill target cells (its effector function) is reduced
- Fas/FasL mediated apoptosis will take over to compensate for perforin deficiency

44
Q

apoptosis via Fas/FasL

A

Fas mechanism can be used to kill the target cell
- FasL is a membrane protein expressed by activated CD8+ T cells
- it binds to its target protein Fas, which is expressed on somatic cells
- interaction results in activation of capsase enzymes resulting in apoptosis of target cell
- target cell debris is removed by macrophages to prevent an inflammatory response

45
Q

CTL killing process review

A
  1. adhesion: LFA-1 : ICAM-1
  2. recognition: TCR: peptide/MHC molecule
  3. movement of granules and reorientation
  4. killing of the target cell: “lethal hit”, pore formation, and cell apoptosis
46
Q

CTL killing cancer cells

A

CTLs can kill cancerous cells in a similar manner
- cancer cells express self-antigens on MHC, allowing CTLs to recognize them

MICR 386 (5 decks)

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