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Immunology Exam I > Innate Immunity > Flashcards

Innate Immunity Flashcards

1
Q

Specificity of Innate Immunity

A

non-specific (preformed)

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2
Q

Kinetics of peak response of innate immunity

A

immediate to early (hours to a few days)

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3
Q

Cells of innate immunity

A

phagocytes (macrophages) , neutrophils, natural killer cells

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4
Q

Cell surface receptors of innate immunity

A

Fc and complement receptors
Lectin (non-polymorphic)
pattern recognition receptors

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5
Q

Circulating molecules of innate immunity

A

complement (non-polymorphic)

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6
Q

Soluble mediators of innate immunity

A

macrophage derived cytokines
other acute phase reactants
systemic effects
inflammation

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7
Q

How is innate immunity amplified

A

recruitment

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8
Q

Does innate immunity have memory

A

no

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9
Q

Specificity of adaptive immunity

A

highly specific (develops)

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10
Q

kinetics of peak response of adaptive immunity

A

later (7-10 days to weeks)

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11
Q

Cells of adaptive immunity

A

T and B lymphocytes

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12
Q

Cell surface receptors of adaptive immunity

A

B and T cell receptors

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13
Q

Circulating molecules of adaptive immunity

A

immunoglobins (diverse)

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14
Q

Soluble mediators of adaptive immunity

A

lymphocyte-derived factors

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15
Q

Amplification of adaptive immunity

A

clonal expansion

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16
Q

does adaptive immunity have memory

A

yes

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17
Q

PRR (pattern recognition receptors)

A

how the innate immune system recorgnizes molecular structures that are produced by microbial pathogens called PAMPs

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18
Q

pathogen-associated molecule patterns (PAMPs)

A

ligands for PRR. one of it’s components is lipopolysaccharide

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19
Q

damage associated molecular patterns (DAMPs)

A

endogenous molecules that are produced by, or released from damaged and dying cells

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20
Q

What does recognition of pathogens via PRR leads to?

A

activation of innate immunity

leads to signal transduction casacade that results in production of proinflammatory cytokines

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21
Q

What cytokines drive inflammation

A

TNF, IL-1, IL-6

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22
Q

What is the anti-viral state driven by

A

interferons

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23
Q

TRL4

A

a toll like receptor that recognizes LPS, meaning it can see gram-negative bacteria

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24
Q

what does hyperactivation of inflammasome result in

A

autoinflammatory syndrome, that can be treated with IL-1 antagonist

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25
Q

Mechanical barrier that helps prevent infection

A

-epithelial cells joined by tight junctions

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26
Q

Chemical barriers that help prevent infection

A
  • defenis and cathelicids which are toxic to microbes
  • low pH
  • antimicrobial enzymes like lysozyme
27
Q

Microbiological barrier to help prevent infection

A

the microbiome (all the bacteria that reside in/on epithelial barriers)

28
Q

Neutrophils

A
  • short lived
  • first cells out to sites of inflammation
  • migrate out of vasculature and into tissues
29
Q

Monocyte/macrophage

A
  • circulate as monocytes in the cell, once they enter the tissue become macrophage
  • long lived
  • found in all tissues
  • tissue resident macrophages may have a different origin than monocyte derived macrophages (yolk sac vs. bone marrow)
30
Q

Dendritic cell

A
  • immature dentric cells exist in tissues
  • highly phagocytic
  • after engulfing pathogens, they migrate to lymph nodes where they downregulate phagocytic capacity and upregulate antigen presentation capacity
31
Q

Opsonins

A

solbule proteins that recognize phagocytic targets, and are in turn recognized by specific receptors on phagocytic cells

32
Q

2 major opsonins in blood

A

complement and antibody

33
Q

Phagosome

A

the vesicle that is formed after a phagocyte engulfs a particle

34
Q

Acidification

A

acidic phagosome fuses with lysosome, killing bacteria

35
Q

Toxic oxygen-derived products

A

superoxide, hydrogen peroxide, singlet oxygen, hydroxyl radial, hypohalite are toxic to microbes

36
Q

Nitric oxide

A

produced from activated macrophages especially following macrophage activation with proinflammatory cytokines such as TNF

37
Q

Lysozyme

A

produced by macrophages. Breaks down cell wall peptidoglycan of bacteria

38
Q

cytokines

A
  • can lead to production of NO

- can leads to activation of lymphocytes

39
Q

Natural Killer Cells

A
  • large, granular
  • don’t specifically recognize antigen
  • kill virus infected cells and certain tumor cells
40
Q

When is NK cell killing activity blocked?

A

when NK cells binds MCH class I on normal cells

41
Q

Exposure to what causes high activation

A

IL-2 or interferons

42
Q

Opsonization

A

coating of microbes with proteins that facilitate phagocytosis.

43
Q

Leukocyte migration

A

chemotaxis stimulated by chemokines

44
Q

Anaphylatoxins

A

complement chemokines.

45
Q

C5a

A

most potent complement anaphylatoxin

46
Q

Lysis of pathogens

A

the terminal components of complement: C5-9 form a pore in the membrane of pathogens (mostly gram neg) resulting in lysis of pathogens

47
Q

gamma-delta T cells

A

monospecific populations in skin and mucosa

48
Q

NKT cells

A

small subset of lymphocytes that express surface molecules characteristics of both NK cells and T cells

  • express TCRs with very little diversity
  • produce cytokines
  • some recognize lipid antigens
49
Q

Functions of complement

A
  • pores in cell surface cause death by osmotic lysis
  • opsonizes antigen to promote phagocytosis
  • produce chemokines to promote inflammation
50
Q

C3’s relationship to complement pathways

A

it is central. Cleaved by C3 convertase which creates C3a and C3b.

51
Q

C3a

A

chemokine that triggers leukocyte recruitment

52
Q

C3b

A

an opsonin that stimulates phagocytosis

53
Q

Classical Complement Pathway

A

initiated by antibody antigen complexes. Two molecules of IgG or one of IgM attaches to a microbial surface to activate. Initiation component is C1

54
Q

Lectin Pathway

A

Initiated by sugar residues that are found on microbial surfaces.

55
Q

Alternative Pathway

A

spontaneous pathway. Low level cleavage of C3 in plasma resulting of generation of C3b that can covalently bind to microbial surface.

56
Q

Paroxysmal nocturnal hemoglobinuria

A

caused by a lack of DAF and CD59

57
Q

Hereditary angioneurotic edema

A

caused by C1 inhibitor deficiency

58
Q

C1 inhibitor

A

restricts the spontaneous activation of C1 in plasma and regulates Hageman factor (which gives rise to HAE)

59
Q

Immune complex disease caused by what deficiency

A

C1, C2, C4

60
Q

What causes bacterial infections, mainly in childhood

A

deficiency of MBL

61
Q

What causes infection with pyogenic bacteria and Neisseria spp. but no immune complex disease

A

Deficiency of Factor D and Factor P

62
Q

What causes infection with pyogenic bacteria and neisseria spp and sometimes immune complex disease

A

C3 deficiency

63
Q

What causes infection with Neisseria spp only

A

deficiency in C5 thru 9

64
Q

Biologic actions of type 1 IFNs

A

inhibit viral replication via a paracrine action
enhance the cytolytic capability of NK cells
increase cellular expression of class I MHC molecules

Immunology Exam I (8 decks)

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