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Immunology Exam I > Innate Immunity > Flashcards

Innate Immunity Flashcards

(64 cards)

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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
Mechanical barrier that helps prevent infection
-epithelial cells joined by tight junctions
26
Chemical barriers that help prevent infection
- defenis and cathelicids which are toxic to microbes - low pH - antimicrobial enzymes like lysozyme
27
Microbiological barrier to help prevent infection
the microbiome (all the bacteria that reside in/on epithelial barriers)
28
Neutrophils
- short lived - first cells out to sites of inflammation - migrate out of vasculature and into tissues
29
Monocyte/macrophage
- 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
Dendritic cell
- 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
Opsonins
solbule proteins that recognize phagocytic targets, and are in turn recognized by specific receptors on phagocytic cells
32
2 major opsonins in blood
complement and antibody
33
Phagosome
the vesicle that is formed after a phagocyte engulfs a particle
34
Acidification
acidic phagosome fuses with lysosome, killing bacteria
35
Toxic oxygen-derived products
superoxide, hydrogen peroxide, singlet oxygen, hydroxyl radial, hypohalite are toxic to microbes
36
Nitric oxide
produced from activated macrophages especially following macrophage activation with proinflammatory cytokines such as TNF
37
Lysozyme
produced by macrophages. Breaks down cell wall peptidoglycan of bacteria
38
cytokines
- can lead to production of NO | - can leads to activation of lymphocytes
39
Natural Killer Cells
- large, granular - don't specifically recognize antigen - kill virus infected cells and certain tumor cells
40
When is NK cell killing activity blocked?
when NK cells binds MCH class I on normal cells
41
Exposure to what causes high activation
IL-2 or interferons
42
Opsonization
coating of microbes with proteins that facilitate phagocytosis.
43
Leukocyte migration
chemotaxis stimulated by chemokines
44
Anaphylatoxins
complement chemokines.
45
C5a
most potent complement anaphylatoxin
46
Lysis of pathogens
the terminal components of complement: C5-9 form a pore in the membrane of pathogens (mostly gram neg) resulting in lysis of pathogens
47
gamma-delta T cells
monospecific populations in skin and mucosa
48
NKT cells
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
Functions of complement
- pores in cell surface cause death by osmotic lysis - opsonizes antigen to promote phagocytosis - produce chemokines to promote inflammation
50
C3's relationship to complement pathways
it is central. Cleaved by C3 convertase which creates C3a and C3b.
51
C3a
chemokine that triggers leukocyte recruitment
52
C3b
an opsonin that stimulates phagocytosis
53
Classical Complement Pathway
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
Lectin Pathway
Initiated by sugar residues that are found on microbial surfaces.
55
Alternative Pathway
spontaneous pathway. Low level cleavage of C3 in plasma resulting of generation of C3b that can covalently bind to microbial surface.
56
Paroxysmal nocturnal hemoglobinuria
caused by a lack of DAF and CD59
57
Hereditary angioneurotic edema
caused by C1 inhibitor deficiency
58
C1 inhibitor
restricts the spontaneous activation of C1 in plasma and regulates Hageman factor (which gives rise to HAE)
59
Immune complex disease caused by what deficiency
C1, C2, C4
60
What causes bacterial infections, mainly in childhood
deficiency of MBL
61
What causes infection with pyogenic bacteria and Neisseria spp. but no immune complex disease
Deficiency of Factor D and Factor P
62
What causes infection with pyogenic bacteria and neisseria spp and sometimes immune complex disease
C3 deficiency
63
What causes infection with Neisseria spp only
deficiency in C5 thru 9
64
Biologic actions of type 1 IFNs
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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