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TERM 3- Postmidterm > DLA24, L39, L41- Cell-Mediated Immunity > Flashcards

DLA24, L39, L41- Cell-Mediated Immunity Flashcards

1
Q

the main cells that important in eliminating viral infections are….

A
  • NK cells (Ag dependent cell mediated cytotoxicity - opsonization)
  • Tc cells (MHC-I)
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2
Q

list the components of humoral immunity in relation to eliminating viral infections (include their effects)

A
  • Igs: opsonizing elements
  • IFN-α/β: produced by virally infected cells to inhibit transcription/translation of neighboring cells
  • IFN-γ: activates macrophages, NK cells, enhances upregulation of MHC-I
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3
Q

describe the fate of a viral antigen

A

Cytosolic Pathway

1) endogenous Ag in cytosol
2) Ag ubiquinated, destroyed by proteosome
3) peptides of Ag into ER via TAP 1/2
4) peptides bind MHC-I
5) MHC-I to golgi then plasma membrane (Ag presentation)

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4
Q

list some viral strategies used to avoid immunity (hint- 6)

A
  • antigenic shift/drift: antigenic variation
  • polymorphism: avoid memory thru different immunological targets
  • latent virus (HSV, VZV)
  • modulation of MHC expression
  • infection of lymphocytes (=> their death)
  • prevention of complement activation
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5
Q

(1) cells are responsible for killing extracellular bacteria. (2) cells are required for Ab response and (3) cells recognize protein/non-protein Ags

A

1- phagocytes
2- Th cells (Th2)
3- B cells

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6
Q

extra cellular bacteria activate complement directly through (1) and (2) pathways where (3) is an opsonin, (4) and (5) recruit leukocytes, and (6) destroy outer membrane of Gram- bacteria

A 
1- lectin
2- alternative
3- C3b
4/5- C3a, C5a (anaphylaxins)
6- MAC (perforates membrane)
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7
Q

_____ is a natural antibacterial of humoral mediated immunity that attacks NAG / NAM links of peptidoglycan => bacterial lysis

A

lysozyme

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8
Q

(1) is the principal defense against extracellular bacteria via (2), (3), (4) mechanisms

A

1- Abs
2- neutralization
3- activation of complement
4- opsonization

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9
Q

(1) and (2) cells are critical to process of cell-mediated immunity of extracellular bacteria

A

1- APCs (Ag presenting cells): macrophages, dendritic cells

2- Th cells (Th1) via MHC-II

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10
Q

describe the fate of a extracellular bacteria antigen

A

Endocytic Pathway

1) exogenous Ags endo-/phago-cytosis into endocytic compartments
2) Ags –> peptides w/in endosome
3) endosome fuses with ER or vesicle with MHC-II
4) Ag replaces CLIP in MHC-II and vesicle goes to surface

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11
Q

describe the role of humoral immunity in regards to intracellular bacteria

A
  • it can bind intracellular bacteria while in transit, before it becomes intracellular
  • ineffective once its intracellular
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12
Q

the main cells that important in eliminating intracellular bacterial infections are….

A
  • NK cells (Ag dependent cell mediated cytotoxicity - opsonization)
  • Tc cells (MHC-I)
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13
Q

list some bacterial strategies used to avoid immunity (hint- 4)

A
  • prevent phagocytosis: destroy phagocytes via toxins, neutralize opsonization
  • survives w/in phagocytes
  • prevent complement activation
  • avoid recognition by immune system via Polymorphism
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14
Q

describe the role of humoral immunity in regards to protozoal infections

A
  • complement / Igs useful during extracellular stage of infection
  • opsonization of protozoa => lysis
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15
Q

the main cells that important in eliminating protozoal infections are….

A
  • NK cells
  • Tc cells

(somewhat phagocytes, Th cells)

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16
Q

list some protozoal strategies used to avoid immunity (hint- 3)

A
  • escape into cytoplasm following phagocytosis
  • prevent complementation
  • gene switching => Ag variation
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17
Q

the most important attack mechanisms against extracellular parasitic worms / helminths is…

A

IgE and complement activation (+ eosinophilic activation)

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18
Q

describe IgE role in helminth parasitic infections

A

activation of granulation of Basophils and Mast cells

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19
Q

(T/F) fungal infections are controlled by innate and adaptive immune systems

A

kinda both: T- few can have Abs, F- vast majority can only be controlled via innate immune system

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20
Q

describe the role of the innate immune system to control fungal infections

A
  • Neutrophilic phagocytosis

- activation of complement (via fungal cell wall components) via alternative and lectin pathways

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21
Q

____ cells have been considered to have a role in elmination fungal infections as a link between their defectiveness and increased fungal infections has been made

A

Th-17 cells (adaptive immunity)- produces IL-17

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22
Q

TCR rearrangement occurs in….

A

thymus- absent when T cell precursor leaves bone marrow

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23
Q

list the APCs

A
  • Dendritic cells (most effective, MHC-II constitutively expressed)
  • Macrophages (activation via phagocytosis before MHC-II expression)
  • B-Cells (MHC-II constitutively expressed)

ALL EXPRESS MHC-II

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24
Q

T cell-mediated immunity only deals with (1) pathogens via expression in (2) or (3) cells and are presented on (4) receptor

A

1- intracellular
2- phagocytic cells (survive w/in phagolysosome / escape into cytosol)
3- non-phagocytic cells (live in nucleus / cytosol)
4- MHC-II

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25
Q

Ags must present to (1) T cells (2) times via APCs before they are activated into (3) T cells

A

1- naive T cells
2- 3 times
3- CD4+/Th or CD8+/Tc cells

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26
Q

list the 4 phases of T cell response to Ags (include the possible resulting cells)

A

1) Ag recognition
2) lymphocyte activation
3) clonal expansion
4) differentiation

Effector Functions: effector Th cell, memory Th cell, effector Tc cell (CTL), memory Tc cell

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27
Q

CD4+ effector T cells function to (1)

CD8+ effector T cells function to (2)

A

1- activation of macrophages, B cells, other cells + inflammation

2- killing infected target cells + macrophage activation

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28
Q

___ is an important CK responsible for advancing a activated lymphocyte into the clonal expansion phase

A

IL-2 (autocrine signaling)

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29
Q

(1) on T cells recognizes peptide shown on APC and (2) recognizes the MHC; (3) is the signal transduction element

A

1- T cell receptors (TCRs)
2- CD4/CD8 (co-receptors)
3- CD3

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30
Q

(1) are important in strengthening the binding of T cells to APCs and (2) from APCs are critical to completely stimulating T cell

A

1- adhesion molecules

2- second signals (co-stimulators)

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31
Q

list the co-stimulators in T cell activation

A

T cell: CD28, CTLA-4, PD-1

APCs: B7-1/2, PD-L1/2

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32
Q

list the adhesion molecules in T cell activation

A

T cell: LFA-1

APCs: ICAM-1

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33
Q

list the 3 polyclonal activators (non-specific)

A
  • Abs for TCR, CD3
  • Carbohydrate-binding proteins
  • superantigens
34
Q

Superantigens are (non-/specific) molecules that cause pathology through (2) by cross-linking (3) and (4); they also include (5) which stimulates cell proliferation

A 
1- non-specific
2- toxic shock syndrome / massive load of CKs
3- MHC-II (APC)
4- VβTCR domain (T cell)
5- T cell mitogens
35
Q

the most important adhesion molecule on T cells is (1) which is apart of the (2) group and binds to (3) on APCs

A

1- LFA-1 (leukocyte function associated antigen)
2- integrins
3- ICAM-1

36
Q

CD28 on (1) cells is a critical co-stimulator that binds to (2) on (3) cells. (4) is present on (1) and (3) cells and is critical in upregulating (2)

A

1- T cells
2- B7
3- APCs
4- CD40L (T cells), CD40 (APCs) [L = ligand]

37
Q

list the members of the B7 family

A

on APCs: B7-1/2, ICOS-L, PD-L1/2

38
Q

list the members of the CD28 family (indicate activators and inhibitors)

A

on T cells:

  • activators: CD28, ICOS
  • inhibitors: CTLA-4, PD-1
39
Q

(1) and (2) molecules on T cells are involved in terminating immune response

A

1- CTLA-4 (binds B7-1/2, opposite effect of CD28)

2- PD-1 (binds PDL-1/2)

40
Q

agents that block B7-CD28 are used in ______ treatment

A

rheumatoid arthritis

41
Q

Abs to CD40-CD40L interaction are being tested for…..

A

graft rejection

42
Q

Abs that block CTLA-4 or PD-1 are used for….

A

enhancing immune response in cancer patients

43
Q

______ interaction is involved in upregulation of B7

A

CD40 (APCs) – CD40L (T cell)

44
Q

describe the role and use for adjuvant in T cell activation

A

binds PRR (protein recognition receptor) on the innate and activate APCs to enhance T cell activation –used in vaccines (which fail to elicit T-cell dependent immune response)

45
Q

after presentation of Ag to Naive T cell, (1) is used to anchor T cell in lymph node, (2) activates T cell into effector T cells which express (3) that is necessary for enhancing 2nd signaling and then finally (4) that is necessary for controlling response

A

1- CD69
2- IL-2 (autocrine signalling)
3- CD40L
4- CTLA-4, PD-1

46
Q

SCID (X-linked) is the result of a the following defect….

A

defect in common γ chain of IL-2R receptor

47
Q

describe briefly how IL-2 works

A
  • Ag stimulated Naive T cell activation
  • IL-2 secreted (autocrine fashion)
  • IL-2Rβγc complex (low affinity) –> IL-2Rαβγc complex (high affinity)
  • => IL-2 induced T cell proliferation
48
Q

HIV is responsible for destroying (1) cells which leads to the inactivation of (2) cells (or the prevention of activation of (2) cells)

A

1- Th CD4+ cells

2- Tc CD8+ cells

49
Q

(1) cells usually require super APCs for activation where (2) do not

A

1- Naive T cells

2- memory T cells (CTLs)

50
Q

list the primary events in CTL-mediated death

A
  • conjugated formation
  • membrane attack
  • CTL dissociation
  • target cell destruction
51
Q

describe the steps of conjugate formation of CTL and a target cell

A
  • Cell Adhesion: LFA-1 (CTL) binds ICAM (target cell)

- Recognition of MHC-I w/ Ag (target cell) via CD8 (CTL)

52
Q

in the Membrane Attack phase on CTLs, granules release (1) first in order to (2) and then (3) is released to act as (4)

A

1- perforins (monomers –> polymer)
2- perforate or put pores in target cell membrane
3- granzymes
4- nucleases

53
Q

CTL cells interact with target cells for (1) and then dissociate (able to conjugate with other target cells) while the target cell dies, which takes (2)

A

1- 5 mins

2- several hrs

54
Q

NK cells defend against the following….

A

viruses, other intracellular pathogens, and tumors

55
Q

NK cells recognize….

A

glycolipid and CD1d

56
Q

activation of NKs is based on (1)

they don’t have the ability to recognize MHCs but can recognize (2)

A

1- balance between activating and inhibitory receptors

2- downregulation MHC receptors (since some viruses can do this) + other alterations in cell surface

57
Q

NK cells can use (1) to induce apoptosis, activate (2) to kill target cells, or respond to (3) surrounding tumor cells

A

1- cytotoxic granules (perforins, granzymes, α-defensins)
2- macrophages (IL-12 –> NK cells –> IFN-γ –> macrophages)
3- Abs (Ab dependent cell mediated toxicity)

58
Q

(1) is an adhesion molecule found on effector Th cells in order to bind to secondary lymphoid tissue. (2) is a chemokine that assists in this process, it also has functions to bring T cell to (3).

A

1- L-selectin
2- CCR7
3- maintain place in paracortex of lymph node (once CCR7 is gone, T cell may migrate ou of paracortex)

59
Q

effector T cells have a (1) role in cell mediated immunity and a (2) role in humoral mediated immunity; it performs this through the expression of (3) on the surface and secretion of (4)

A

1- activate phagocytes (macrophages, neutrophils)
2- activate B cells
3- CDL40
4- CKs

60
Q

Intracellular microbes are presented via (1) or (2) cells to naive T cells. (1) will secreted (3) and (2) secreted (4) for activation to occur, and the naive T cell will mature into (5). This is considered (cell/humoral) mediated immunity.

A

1/3- dendritic cell, IL-12
2/4- NK cell, IFN-γ
5- Th1 cell
6- cell mediated immunity

61
Q

list the products and functions of Th1 secretions

A
  • IFN-γ: macrophage activation, O2-dep./indep. mechs, respiratory burst, NO
  • IL-12: O2-indep. mechs
  • IL-2: Th1 target
  • TNF-α: inflammation
62
Q

Helminths are presented via (1) cells to naive T cells and secretes (2) for activation to occur. The naive T cell will mature into (3). This is considered (cell/humoral) mediated immunity.

A

1- mast cells / eosinophils (mainly, could be dendritic cells)
2- IL-4
3- Th2 cell
4- humoral mediated immunity

63
Q

list the products and functions of Th2 secretions

A
  • IL-4: IgE production, basophil/mast cell activation
  • IL-5: eosinophil activation
  • IL-10: inhibit Th1
  • IL-25: activate the above CKs
64
Q

Extracellular bacteria and fungi are presented via (1) cells to naive T cells and secrete the following, (2), to activate and mature the T cell into (3), which secretes the following CKs, (4).

A

1- dendritic cells
2- IL-1, IL-6, IL-23, TGF-β
3- Th17 cells
4- IL-17, IL-21, IL-22

65
Q

Treg cells secrete (1) and (2) for the function to (3)

A

1- TGF-β
2- IL-10
3- immunoregulation (suppresor)

66
Q

Tfh, aka (1), secretes (2) and other CKs in order to (3)

A

1- T follicular helper cell
2- IL-21
3- activate B cells

67
Q

IFN-γ stimulates phagocytic mediated ingestion through (1) and (2). To promote phagocytosis it stimulates the expression of (3). To amplify T cell response it stimulates (4). It also activates macrophages to produce (5) in order to (6).

A

1- expression of lysosomal proteases
2- synthesis of ROS and NO (deal with organisms that escape phagosome)
3- Ab production
4- MHC-II and B7 expression on APCs
5- IL-12
6- drive Th1 cell production (amplification)

68
Q

describe the 3 signals in a Th1 cell - macrophage interaction

A

1) CD4 (T cell) + MHC / co-stimulators (macrophages)
2) CD40L (T cell) + CD40 (macrophage)
3) IFN-γ (T cell) + IFN-γ Receptor (macrophage)

69
Q

Th1 cell activation leads to the following three responses from macrophages

A
  • killing phagocytosed bacteria (via ROS + NO)
  • increased MHC + co-stimulator (B7) expression
  • CK secretion: TNF-α, IL-1, IL-12
70
Q

Th2 cells produce IL-4 for (1) production, where (1) coats (2) so (3) cells can kill them through release of granules enzymes. IL-5 is produced in order to (4).

A

1- IgE
2- parasites
3- eosinophils / mast cells
4- activate eosinophil

71
Q

Th2 cell produce these three CKs, (1), to have alternative (2) activation in order to (3) and (4).

A

1- IL-4, IL-10, IL-13
2- macrophage (M2) [IL-10]
3- synthesis of extracellular proteins for repair
4- inhibit microbicidal activity of macrophages (suppress Th1)

72
Q

classically activated macrophages (M1) are stimulated by (1) and have (2) and (3) as functions

alternatively activated macrophages (M2) are stimulated by (4) with (5) as its function

A

1- IFN-γ, TLR-ligands
2- microbicidal actions: phagocytosis / killing of bacteria/fungi
3- inflammation

4- IL-4, IL-13
5- antiinflammatory effects, wound repair, fibrosis

73
Q

high Th1 has the internal threat of (1) and low Th1 has the internal threat of (2)

A

1- autoimmune issue (immune over-reaction)

2- cancer (immune under-reaction)

74
Q

high Th2 has the external threat of (1) and low Th2 has the external threat of (2)

A

1- allergic reaction (immune over-reaction

2- infection (immune under-reaction)

75
Q

mycobacterium leprae infections can have a dominant Th1 reaction leading to (1) or dominant Th2 reaction (or defective Th1) leading to (2)

A

1- tuberculoid leprosy (less severe)

2- lepromatous leprosy (more severe

76
Q

Th17 cells function to destroy (1) and it defect would lead to (2)

A

1- fungal and extracellular bacteria

2- bacterial abscess, chronic mucocutaneous candidiasis (many fungal infections)

77
Q

Th17 cells induce (1) and stimulates production of (2) antimicrobial. There most important CKs are (3) and (4) [include function of CKs]

A

1- inflammation
2- defensins
3- IL-17 –> recruits leukocytes / neutrophils (–> inflammation + antimicrobial peptides)
4- IL-22 –> maintains epithelial barrier integrity (+ antimicrobial peptides)

78
Q

memory T cells found in lymphoid organs are called (1) and if found in peripheral tissue are called (2)

A

1- central memory T cells, rapid clonal expansion

2- (mucosa/skin) effector memory T cells, rapid effector cell

79
Q

memory T cells (effector or central) are in the (1) phase of the cell cycle, require (2) to stay alive, have a (3) life-span compared to effector T cells, and are responsible for (4)

A

1- Go (quiescent) stage
2- IL-7
3- mos-yrs vs days-wks
4- secondary response to pathogens

80
Q

describe the result of cell production after an acute viral infection vs a chronic infection

A

Acute- memory T cells, protective response to virus

Chronic- exhausted T cells, unable to respond to virus due to PD-1, CTLA-4 inhibition

81
Q

define T cell anergy and its causes

A

Clonal Anergy:

  • inability of cells to proliferate in response to MHC-peptide complex
  • caused by absence of costimulatory signal OR presence of CTLA-4, PD-1 (inhibitory signals)
82
Q

list 5 ways for microbes to resist cell-mediated immunity

A
  • inhibit fusion of phagosomes and lysosomes
  • inhibit Ag / MHC-I expression
  • inhibit macrophage activation
  • inhibit CK activation of T cells (neutralize CKs someway)
  • directly infect T cells (ex. HIV)

TERM 3- Postmidterm (11 decks)

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