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MAD Exam 2 > Innate Immunity > Flashcards

Innate Immunity Flashcards

1
Q

peripheral (secondary) immune system organs

A

lymph nodes & spleen
*where cells RESIDE

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2
Q

central (primary) lymphoid organs

A

bone marrow & thymus
*where immune cells are MADE

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3
Q

cells of innate immunity

A

NK cells
neutrophils
eosinophils
basophils
dendritic cells
mast cells
monocytes
mast cells

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4
Q

cells of adaptive immunity

A

lymphocytes (B & T cells)
plasma cells

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5
Q

lymphocytes

A

production of antibodies (B cells) or cytotoxic and helper functions (T cells)

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6
Q

plasma cells

A

fully differentiated form of B cell that secretes antibodies
*live in the spleen and bone marrow

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7
Q

natural killer (NK) cells

A

kills cells infected with certain viruses

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8
Q

neutrophils

A

phagocytosis and killing of microorganisms (especially BACTERIA)

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9
Q

eosinophils

A

killing of antibody-coated parasites through release of granule contents

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10
Q

basophils

A

controlling immune response to parasites

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11
Q

mast cells

A

expulsion of parasites from body through release of granules containing histamine and other active agents

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12
Q

monocytes

A

circulating precursor to macrophage

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13
Q

macrophages

A

phagocytosis and killing of microorganisms; activation of T cells and initiation of immune response

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14
Q

dendritic cells

A

responsible for T cell activation and initiation of adaptive immune responses
*interaction between innate and adaptive immunity

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15
Q

innate immunity

A

-physical barriers (skin, mucous membranes)
-cells (neutrophils, macrophages, dendritic cells)
-complement
-rapid in onset
-antigen-nonspecific
-initiates events required for adaptive immune response
-no memory

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16
Q

adaptive immunity

A

-cell mediated immunity (T cells)
-antibody producing B cells
-requires several days
-highly antigen-specific
-exhibits immunologic (antigen-specific) memory

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17
Q

3 main functions of innate immunity

A

1) initiate a rapid response against the pathogen
2) limit the spread of infection
3) initiate the adaptive immune response at secondary lymphoid site (e.g. draining a lymph node

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18
Q

how does the innate immune system initiate the adaptive immune system

A

innate antigen-presenting cells (dendritic cells & macrophages) will:
1) carry the antigen from the site of infection to a secondary lymphoid site, like a nearby draining lymph node
2) present the antigen to clones of T and B lymphocytes that reside in secondary lymphoid site
3) once T cells are activated, they can traffic to the site of infection from lymph nodes and the bloodstream in order to help clear the pathogen

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19
Q

acute inflammation

A

reaction of the innate immune system that serves as a transient, early response to infection or injury
s/s include:
-rubor (redness)
-calor (heat)
-tumor (swelling)
-dolor (pain)

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20
Q

components of acute inflammation

A

a) vascular: vasodilation and increased endothelial permeability (allows cells out of blood into the infected tissue)
b) cellular: extravasation of leukocytes (4 steps: margination and rolling, adhesion, diapedesis, migration)

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21
Q

when will neutrophils peak during acute inflammation

A

at about 24 hours

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22
Q

when will macrophages peak during acute inflammation

A

at about 2-3 days

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23
Q

possible outcomes of acute inflammation, influenced by cytokines from macrophages

A

1) resolution and healing (IL-10 and TGF beta)
2) persistent acute inflammation (IL-8: pro-inflammatory)
3) abscess - acute inflammation walled off by fibrosis
4) chronic inflammation - APCs activate CD4+ Th cells
5) scarring

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24
Q

type I interferons

A

*proteins made by the innate immune system
*bind to IFNAR (interferon alpha/beta receptor), expressed by almost every cell
*puts the cell into an anti-viral state

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25
Q

effectors of innate immunity

A

cytokines
acute phase reactants
phagocytes
natural killer cells
innate lymphoid cells (ILCs)

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26
Q

cytokines

A

proteins that communicate between cells of the immune system and between immune cells and other cells of the body
*interferons are a type of cytokine

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27
Q

acute phase reactants

A

facilitate a range of processes involved in pathogen clearance
*produced by the liver

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28
Q

phagocytes (neutrophils, macrophages, dendritic cells) as effectors of innate immunity

A

engulf and destroy bacterial pathogens

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29
Q

innate lymphoid cells (ILCs)

A

lymphoid cells that lack an antigen receptor; produce cytokines

30
Q

positive acute phase reactants

A

*tend to be increased during inflammation
ferritin
fibrinogen
serum amyloid A
hepcidin
C-reactive protein

31
Q

ferritin

A

positive acute phase reactant
*binds and sequesters IRON

32
Q

negative acute phase reactants

A

*tend to be downregulated during infection
albumin
transferrin

33
Q

transferrin

A

negative acute phase reactant
*internalized by macrophages to sequester IRON

34
Q

4 part response of innate immunity to BACTERIA

A
  1. activation of the complement system
  2. recruitment of neutrophils and macrophages
  3. induction of cytokine synthesis by resident macrophages, endothelial and epithelial cells
  4. maturation of dendritic cells
35
Q

C3a

A

anaphylatoxin
*recruits inflammatory components from vascular space

36
Q

C3b

A

opsonin
*coats bacterium to enhance phagocytosis

37
Q

functions of C3b

A
  1. a component of the C3 convertase
  2. opsonin: a modified form of C3b termed iC3b promotes phagocytosis by macrophages and neutrophils
  3. a component of the C5 convertase
38
Q

C5b

A

component of the membrane attack complex

39
Q

C5a

A

the most potent anaphylatoxin
*a chemotactic factor for neutrophils

40
Q

C3a and C5a

A

anaphylatoxins
*result in:
-increased flow of circulating complement components to the site of infection
-recruitment of phagocytes via adhesion molecules

41
Q

decay accelerating factor

A

*expressed by host cells
*competes with Factor B for binding to C3b
**prevents positive feedback loop of C3 convertase formation (helping us not be attacked by our own complement system)

42
Q

factor H

A

*preferentially binds host cell due to sialic acid on surface
*can displace Factor B from C3b, making C3b available for proteolysis
*Factor I lyses (degrades) free C3b
(helping us not be attacked by our own complement system)

43
Q

paroxysmal nocturnal hemoglobinuria - disease overview

A

complement-mediated intravascular RBC lysis

44
Q

paroxysmal nocturnal hemoglobinuria - pathophysiology

A

impaired DAF/Cd55 -> RBC membrane unprotected from complement

45
Q

paroxysmal nocturnal hemoglobinuria - labs

A

CD55 (-) RBCs on flow cytometry

46
Q

paroxysmal nocturnal hemoglobinuria - treatment

A

eculizumab - inhibits terminal complement formation

47
Q

factor I deficiency

A

leads to low levels of circulating C3
*consumptive deficiency: without factor I, C3 convertase is uninhibited, leading to a high rate of C3 consumption, leading to increased pyogenic infections

48
Q

toll-like receptors

A

*family of cell surface proteins that are involved in the RECOGNITION of microbial pathogens and activation of the innate immune response
*recognize PAMPs (patterns, rather than unique ligands)

49
Q

molecules recognized by TLR1 and TLR 6

A

components of gram-positive bacteria

50
Q

molecules recognized by TLR 2

A

components of gram-positive bacteria

51
Q

molecules recognized by TLR 3

A

double stranded RNA

52
Q

molecules recognized by TLR 4

A

LPS (lipopolysaccharide), pili, RSV F protein

53
Q

molecules recognized by TLR 5

A

gram-negative flagellin

54
Q

molecules recognized by TLR 9

A

unmethylated CpG DNA (abundant in bacteria)

55
Q

TLR signaling

A

1) TLR agonists bind to receptors on macrophages and neutrophils at the site of infection
2) agonist stimulates the cells to make pyrogens (IL-1, IL-6, and TNF alpha) and chemokines
3) pyrogens cause increased expression of ADHESION MOLECULES on the circulating neutrophils, monocytes, and endothelial cells
4) adhesion, together with the chemokines, causes increases in neutrophil and monocyte infiltration at the site of infection
5) the neutrophils use C3b to enhance their ability to phagocytose bacteria

56
Q

respiratory burst

A

KEY ENZYME: NADPH oxidase
*the destruction of internalized bacteria is mediated by reactive oxygen species (ROS), including nitric oxide (NO), superoxide, hydrogen peroxide, and hypochlorite
*ROS are produced in phagocytes like neutrophils and kill the bacteria

57
Q

chronic granulomatous disease (CGD)

A

deficiency in NADPH oxidase, causing failure of the respiratory burst to kill bacterial pathogens

58
Q

TNF-alpha functions

A

fever, sepsis, WBC recruitment; maintains granulomas is TB; causes cachexia in malignancy

59
Q

IL-1 functions

A

fever, acute inflammation (aka osteoclast-activating factor)

60
Q

IL-6 functions

A

fever, acute phase reactants

61
Q

IL-8 functions

A

major chemotactic factor for neutrophils

62
Q

IL-12 functions

A

induces Th1 cells; activates NK cells

63
Q

why are pyrogens beneficial for our immune response

A

increased body temperature helps the immune cells work better, as well as hindering pathogen functions

64
Q

dendritic cell maturation

A

TLR ligands bind to TLRs on dendritic cells, inducing MATURATION and MIGRATION of the dendritic cells to secondary lymphoid sites (spleen, lymph nodes), where they promote antigen-specific activation of T cells

65
Q

4 part response of innate immunity to VIRUSES

A

1) production of Type I interferons*
2) recruitment of natural killer cells*
3) induction of cytokine synthesis by resident macrophages, endothelial and epithelial cells
4) maturation of dendritic cells

66
Q

innate immune response to a virus

A

*type I interferons (IFN-alpha and IFN-beta) are produced by infected cells, leading to dendritic cell maturation and NK cell recruitment
*specific viral proteins and double-stranded RNA can signal via TLRs
*double-stranded viral RNA can also signal through cytoplasmic pattern recognition receptors such as RIG-1 and MDA5

67
Q

how do interferons work to put a cell in the anti-viral state

A

1) downregulate protein synthesis to resist potential viral replication
2) upregulate MHC expression to facilitate recognition of infected cells
**protects the NEIGHBORING cells, not really the infected cell

68
Q

activation of NK cells

A

1) exposed to nonspecific activation signal on target cell or MIC ligand
2) exposed to ABSENCE of MHC1 on target cell surface
3) antibody-dependent cell-mediated cytotoxicity; CD16 of NK binds Fc region of antibody to activate NK cell

69
Q

how do NK cells kill infected cells

A

induce apoptosis in virally-infected cells with:
*perforin (perforate the membrane)
*granzymes (proteases, which cleave cellular proteins, especially pro-caspase 9)

70
Q

which bacterial pathogens are people with CGD most susceptible to

A

catalase-positive organisms

MAD Exam 2 (37 decks)

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