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Microbiology > 2. Innate Immunity, Cell Migration, and Phagocytosis > Flashcards

2. Innate Immunity, Cell Migration, and Phagocytosis Flashcards

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1
Q

innate (constitutive) response is the __ response to injury; mediated mainly by __ cells, also __ and __ __ __; has some specificity and no __.

A

initial, myeloid, NK, innate lymphoid cells (ILC), memory

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2
Q

adaptive response is mediated by __ __ ___ (T and B cells); highly specific for __; has __; takes a long time to get started

A

clonally selectable lymphocytes, antigens, memory

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3
Q

innate immunity response time

A

hours

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4
Q

innate immunity specificity

A

limited and fixed “pattern recognition”

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5
Q

innate immunity response to repeat infections

A

always the same

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6
Q

innate immunity major components

A
  • physical barriers
  • phagocytes
  • pattern recognition receptors
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7
Q

innate immunity genes

A

constitutive

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8
Q

adaptive immunity response time

A

days-weeks

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9
Q

adaptive immunity specificity

A

diverse, improves during response

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10
Q

adaptive immunity response to repeat infections

A

faster, stronger, longer-lasting

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11
Q

adaptive immunity major components

A
  • T and B cells
  • antigen-specific receptors
  • antibodies
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12
Q

adaptive immunity genes

A

altered by somatic recombination (VDJ)

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13
Q

5 physical barriers

A
  • skin: acidic, anti-microbial peptides
  • mouth: enzymes, anti-microbial peptides, directional flow of fluid to stomach
  • stomach: low pH, digestive enzymes, fluid flow to intestine
  • intestine: mucus, anti-microbial peptides, normal microbiota compete for niches
  • airways and lungs: cilia, mucus, anti-microbial peptides, coughing/sneezing
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14
Q

4 steps of early immune/inflammatory responses

A
  1. tissue damage causes release of vasoactive and chemotactic factors that trigger a local increase in blood flow and capillary permeability
  2. permeable capillaries allow an influx of fluid (exudate) and cells
  3. phagocytes migrate to site of inflammation (chemotaxis)
  4. phagocytes and antibacterial exudate (complement, C-reactive protein) destroy bacteria
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15
Q

4 main innate immune cell types

A
  • neutrophils
  • macrophages
  • dendritic cells
  • natural killer cells
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16
Q

3 functions of neutrophils

A
  • phagocytosis
  • reactive oxygen and nitrogen species
  • antimicrobial peptides
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17
Q

6 functions of macrophages

A
  • phagocytosis
  • inflammatory mediators
  • antigen presentation (to T cells) (less effective than DC)
  • reactive oxygen and nitrogen species
  • secrete inflammatory cytokines and other mediators
  • complement proteins
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18
Q

5 functions of dendritic cells

A
  • antigen presentation (to T cells)
  • costimulatory signals
  • reactive oxygen species
  • interferon
  • cytokines
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19
Q

3 functions of natural killer cells

A
  • lysis of viral-infected cells
  • interferon
  • macrophage activation
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20
Q

these cells are the first line of defense (earliest cells recruited to infected or wounded site)

A

neutrophils

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21
Q

neutrophils doing phagocytosis

A
  • foreign microbes are engulfed into phagosomes
  • more efficient if microbes are opsonized by Abs and/or complement
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22
Q

neutrophils doing killing

A
  • oxidative: ROS and RNS
  • non-oxidative: cationic proteins, enzymes
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23
Q

IFNgamma cytokines can activate which cell type

A

macrophages

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24
Q

which cell type is the main APC in primary immune response (in peripheral tissue, esp skin and mucosae)

A

dendritic cells

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25
Q

these cells are phagocytic cells (related to macrophages?) that ingest microbes, Ag through innate receptors

A

dendritic cells

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26
Q

TLR signals activate dendritic cells to do 3 things:

A
  • upregulate MHC-II (presents processed Ag peptide to T cells)
  • upregulate T-cell co-stimulatory molecules (CD40L, CD80, CD86)
  • induce migration to draining lymph nodes
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27
Q

how do macrophages, dendritic cells, and other innate immune cells recognize foreign microbes in a naive host before adaptive responses have developed?

A

patterns (recognized on receptors)

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28
Q

TLR (cell surface or internal compartments) target/source

A

microbial components not found in hosts

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29
Q

TLR (cell surface or internal compartments) effect of recognition

A

induces innate response

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30
Q

where was the gene for Toll first found? and what does it do?

A

drosophila; directs dorsal-ventral axis formation

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31
Q

TLR are also known as

A

pattern recognition receptors (PRR); they distinguish microbes from host cells (recognize patterns)

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32
Q

true or false: TLR recognize microbial components not found in the host

A

true

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33
Q

true or false: TLR are not critical for immunity

A

false; TLR are critical for immunity!

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34
Q

3 examples of TLR

A
  • TLR4 recognizes lipopolysaccharride (LPS) on gram-negative bacteria
  • TLR5 recognizes bacterial flagellin
  • various intracellular TLRs recognize ss or ds (viral) RNA, bacterial DNA (CpG motifs)
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35
Q

TLR structure

A

leucine-rich repeats on extracellular domain recognize ligands

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36
Q

TLR signaling

A

“TIR” domain (box 1, 2, 3) on cytoplasmic domain activates inflammatory signaling pathways

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37
Q

TLRs activate two pathways:

A
  • extracellular pathogens: activate “MyD88-dependent” pathway –> turn on pro-inflammatory cytokines (TNFalpha, IL-1, IL-6)
  • intracellular pathogens: activate anti-viral cytokines –> turn on IRF transcription factors and lead to expression of type I interferons (IFNs)
38
Q

which pathway do most TLRs signal through?

A

MyD88

39
Q

what is NF-kB

A

an inflammatory transcription factor

40
Q

multiple inflammatory signals converge on __ which binds to promoter elements in target pro-inflammatory genes such as:

A

blank: NF-kB

  • inflammatory cytokines: IL-1, IL-6, TNFalpha
  • proteins that facilitate antigen presentation and T cell activation
  • acute phase response genes
  • anti-microbial proteins
  • other inflammatory mediators: prostaglandins, iNOS
41
Q

intracellular PRR (pattern recognition receptor)

A

nucleotide-binding oligomerization domain (NOD) proteins

42
Q

what do NODs do?

A
  • recognize microbial components found in cytosol
  • bind peptidoglycan in bacterial cell walls
  • lead to activation of caspase-1 –> cleavage of inactive forms of IL-1
  • mutations in NOD genes associated with inflammatory bowel disease, asthma
43
Q

types of interferons (IFNs)

A
  • IFN-gamma
  • IFN-alpha
  • IFN-beta
44
Q

IFN-alpha and IFN-beta (type 1 interferons) have direct ___ activity

A

anti-viral

45
Q

IFN-alpha and IFN-beta activate genes that __ polyA mRNA and __ initiation of mRNA translation

A

degrade, inhibit

46
Q

which IFN is the “immune interferon”

A

IFN-gamma

47
Q

what does IFN-gamma activate

A

NK cells and macrophages

48
Q

what does IFN-gamma upregulate

A

MHC-II on APC

49
Q

what is IFN-gamma made by

A

CD4+ Th1 cells, CD8+ T cells, NK cells

50
Q

general steps of inflammation and local response

A
  • activated innate cells trigger inflammation
  • acute vs chronic
  • local vs systemic
  • inflammatory cytokines (recruit other cells to the site, trigger systemic innate defenses)
51
Q

systemic acute phase response

A

local inflammatory response accompanied by systemic APR

52
Q

what occurs in systemic APR

A
  • fever
  • ACTH and hydrocortisone production increases
  • acute phase proteins synthesized by the liver
    • C-reactive proteins promote phagocytosis of microbes
    • complement proteins
    • fibrinogen, MBP, serum amyloid A, etc
  • induced by inflammatory cytokines
    • IL-6, TNFalpha, IL-1
53
Q

types of antimicrobial peptides

A
  • defensins
  • cathelicidins (LL-37)
  • S-100 proteins (calprotectin)
  • Reg-IIIgamma
  • Lipocalin-2
54
Q

defensins

A
  • small cationic peptides (~20 kDa) typically found in mucosal secretions (gut, mouth, etc)
  • directly kill microbes
  • similar proteins found in frogs, invertebrates, plants, etc.
55
Q

other innate antimicrobial factors

A
  • lysozyme
  • lactoferrin
  • peroxidase
  • histastins
    *all found in saliva
56
Q

lysozyme as an antimicrobial factor

A
  • muramidase hydrolyses bacterial peptidoglycan
  • cationic protein (pI > 10)
57
Q

lactoferrin as an antimicrobial factor

A

binds free iron down to pH 4

58
Q

peroxidase as an antimicrobial factor

A

uses H2O2 to oxidize SCN- to OSCN-; inhibits bacterial metabolism

59
Q

histatins as an antimicrobial factor

A

small His-rich peptides are active against Candida

60
Q

interplay of innate and adaptive immune systems

A
  • TLRs recognize components on microbes (triggers release of inflammatory cytokines like TNFalpha, IL-1, IL-6, IL-8; upregulates costimulatory molecules on APC –> activate T cells)
  • DC ingest bacteria, present antigens to T cells
  • TNFalpha and IL-8 upregulate adhesion molecules on vascular endothelium –> recruit neutrophils and lymphocytes
  • cytokines secreted by various cells shape the T cell response
61
Q

what is IL-12 secreted by and how does it shape the T cell response?

A
  • secreted by macrophages and dendritic cells
  • Th1: antibacterial Ab and CMI
62
Q

what is IL-4 secreted by and how does it shape the T cell response?

A
  • secreted by mast cells
  • Th2: mainly antiparasitic immunity
63
Q

what is IL-6 secreted by and how does it shape the T cell response?

A
  • secreted by macrophages
  • Th17: immunity to fungi, extracellular bacteria
64
Q

what is TGFbeta secreted by and how does it shape the T cell response?

A
  • secreted by many cells
  • Th17: immunity to fungi, extracellular bacteria
  • Treg: immune regulation
65
Q

involvement of ___ links innate immunity to adaptive immunity

A

TLR

66
Q

what is cell migration induced by

A

injury (vasoactive and chemotactic factors are released in response to bacteria from tissue damage injury)

67
Q

immune cell migration is a property common to all __, is preferential __ of different cells to different sites, and is essential for the capacity of the immune system to protect __

A

leukocytes, migration, tissues

68
Q

3 steps in neutrophil migration (emigration of neutrophils from circulation into tissues)

A
  • cell “rolling” (adhere to endothelium instead of floating by; think of velcro shoes on velcro floor)
  • firm adhesion (tight binding)
  • diapedesis (skeletal changes to squeeze through the wall
    *all steps are catalyzed by a variety of adhesion molecules
69
Q

4 steps of lymphocyte migration

A
  1. naive lymphocytes move from primary lymphoid tissues, via circulation, to secondary lymphoid tissues (this is where Ag processing and presenting)
  2. activated lymphocytes move from spleen and lymph nodes into circulation
  3. circulating activated lymphocytes migrate into other lymphoid organs, or cross vascular endothelium into other tissues
  4. antigen presenting cells migrate to lymphoid organs, carrying antigen from the periphery
70
Q

chemotaxis is the

A

directed movement of leukocytes along a concentration gradient of chemoattractants

71
Q

chemoattractants may be derived from

A

the tissue or from infecting organisms

72
Q

chemotaxis stimulates

A

leukocytes by binding to receptors on the neutrophil surface

73
Q

4 examples of neutrophil chemoattractants

A
  • N-formyl-methionyl peptides (FMLP)
  • complement fragment C5a
  • leukotriene B4 (LTB4)
  • interleukin-8
74
Q

adhesion molecule numbers can be modulated by

A
  • recruitment from intracellular stores
  • novel synthesis
  • both
75
Q

3 families of adhesion molecules

A
  • immunoglobulin superfamily (Ab, TCR, MHC, T cell components, etc)
  • integrins
  • selectins
76
Q

3 major beta2-integrins (very important adhesion molecules!)

A
  • CD11a/CD18 (aka LFA-1)
  • CD11b/CD18 (aka Mac-1)
  • CD11c/CD18 (aka p150,95)
    *CD18 subunit is critical to these integrins
77
Q

what is CD11a/CD18 (LFA-1) expressed by

A

T and B cells, NK cells, granulocytes, and macrophages

78
Q

what are the ligands for CD11a/CD18 (LFA-1)

A

ICAM-1 and ICAM-2

79
Q

what does LFA-1 mediate

A

it mediates the adhesion of T cells to various other cell types including APC

80
Q

what are CD11b/CD18 (Mac-1) and CD11c/CD18 (p150,95) expressed by

A

myeloid cells but not by the majority of T cells

81
Q

what are the ligands for CD11b/CD18 (Mac-1) and CD11c/CD18 (p150,95)

A

C3Bi and others

82
Q

what do CD11b/CD18 (Mac-1) and CD11c/CD18 (p150,95) play an important role in

A

adhesion and emigration of leukocytes to extravascular sites

83
Q

leukocyte adherence deficiency is a defect in

A

the gene for CD18

84
Q

leukocyte adherence deficiency causes

A

defective expression of all three beta2-integrins at the cell surface

85
Q

leukocyte adherence deficiency results in

A

clinical condition, often fatal

86
Q

during opsonization, __ are activated by __, via specific surface receptors for __

A

phagocytes, immunoglobulins, Fc

(FcgammaR (I, II, III); FcalphaR)

87
Q

in opsonization, distinction of bound from free Ig is achieved through __ binding of Igs on __ surface (i.e. crosslinking of FcR)

A

multivalent, Ag

88
Q

what receptors are involved in opsonization

A

complement, CR3 (CD11b/CD18 - Mac-1)

89
Q

6 steps in phagocytosis

A
  1. adherence (enhanced by opsonins)
  2. ingestion (uptake into phagosome)
  3. fusion of lysosomes to form phagolysosome
  4. activation of respiratory burst
  5. destruction and digestion by lysosomal contents and reactive oxygen species
  6. exocytosis of remains (APC will save some remains and give to T cells)
90
Q

3 steps of respiratory burst

A
  1. increase in oxidative metabolism of phagocytes following uptake of opsonized particles (NADPH, oxidized to generate O2-)
  2. production of bactericidal reactive oxygen/nitrogen intermediates (O2- –> H2O2; iNOS –> NO)
  3. myeloperoxidase uses H2O2 to oxidize Cl- to OCl-

Microbiology (7 decks)

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