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Immunology > Chapter Three > Flashcards

Chapter Three Flashcards

1
Q

What is the difference between the lymphoid & myeloid lineages?

A

lymphoid progenitor creates immune cells (plasma, T cell, NK) myeloid progenitor creates tissue cells (mast cells, macrophages)

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2
Q

What are PRRs?

A

pattern recognition receptors that recognized pathogen associated molecular patterns (PAMPs) or damaged associated molecular patterns (DAMPs) from stressed cells

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3
Q

What kind of recognition molecules does the innate immune system use?

A

germline-encoded receptors

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4
Q

What kind of recognition molecules does the adaptive immune system use?

A

antigen receptors of unique specificity assembled from incomplete gene segments during lymphocyte development

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5
Q

What are the 4 main groups of PRRs?

A
  1. free receptors in the serum (ex: ficolins, histatins) 2. membrane bound phagocytic receptors 3. membrane bound signaling receptors 4. cytoplasmic signaling receptors
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6
Q

What are the main classes of phagocytic cell in the innate immune system?

A
  1. macrophages (tissue) & monocytes (blood) 2. granulocytes 3. dendritic cells
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7
Q

What is the major phagocyte population that is resident in most normal tissues at homeostasis?

A

macrophages

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8
Q

What are macrophages in neural tissue called?

A

microglial cells

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9
Q

What are macrophages in the liver called?

A

Kupffer cells

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10
Q

What are the different granulocytes?

A
  1. neutophils (most active) 2. eosinophils 3. basophils
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11
Q

What are PMNs?

A

polymorphonuclear neutrophilic leukocytes (aka polys): neutrophils. short lived cell that are abundant in the blood but no present in healthy tissues

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12
Q

What do immature dendritic cell reside?

A

lymphoid organs & peripheral tissues. primarily branch from cells of myeloid potential

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13
Q

How are dendritic cells different from macrophages & neutrophils?

A

they ingest & break down microbes but their primary role is not front-line, large-scale direct killing of microbes

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14
Q

What are the 2 functional types of dendritic cells?

A
  1. conventional (or classical) dendritic cells (cDCs) 2. plasmacytoid dendritic cells (pDCs)
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15
Q

What do cDCs do?

A
  1. process ingest microbes in order to generate peptide antigens that can activate T cells & induce an adaptive immune response 2. produce cytokines in response to microbial recognition that activate other types of cells against infection
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16
Q

Why are cDCs important?

A

bridge between innate & adaptive immune responses bc they produce cytokines

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17
Q

What do pDCs do?

A

produce class of cytokines known as type I interferons (antiviral interferons) & are considered to be part of innate immunity

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18
Q

What is the macrophage mechanism?

A
  1. macrophage receptors bind microbes & their components 2. bound material is internalized in phagosomes & broken down in phagolysosomes
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19
Q

What do GPCRs on phagocytes do?

A

link microbe recognition w/ increased efficiency of intracellular killing

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20
Q

How is the microbicidal respiratory burst in phagocytes initiated?

A

activation-induced assembly of the phagocyte NADPH oxidase allows ROS-reactive oxygen to breakdown bacteria

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21
Q

What does GPCR activate?

A

heterotrimeric G protein: the beta & gamma parts activate other signaling pathways

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22
Q

What are NETs? What do they do?

A

neutrophil extracellular traps (NETs) - trap bacteria & fungi

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23
Q

What happens when microbes & tissue macrophages interact?

A

macrophages & other immune cell become activates and release cytokines and chemokines

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24
Q

What do cytokines & chemokines do?

A
  1. induce inflammation in the tissue 2. attract monocytes & neutrophils to the infection & allow plasma proteins to enter the tissue from the blood
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25
Q

What is TNF-alpha?

A

(tumor necrosis factor) pro-inflammatory cytokine secreted by macrophages & induces secretion of lipid mediators

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26
Q

What are the 3 essential roles of inflammation?

A
  1. addition supply (demand vs. supply) - deliver additional effector molecules 2. induce physical barrier for pathogen & local blood clotting 3. repair injured tissue
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27
Q

How is inflammation characterized?

A
  1. increased in vascular diameter -> increased BF -> heat & redness 2. change in activation of endothelial cells lining the BV to express cell adhesion molecules that promote the binding of circulating leukocytes 3. extravasation - leukocytes attach to endothelium & migrate into the tissues
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28
Q

What does infection stimulate?

A

macrophages to release cytokines & chemokines that initiate an inflammatory response

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29
Q

Once inflammation begins, what are the WBCs attracted to the site?

A

neutrophils

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30
Q

What are the 2nd WBCs attracted to the site of infection?

A

monocytes

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31
Q

What happens to monocytes after they are activated?

A

become inflammatory monocytes & can produce various pro-inflammatory cytokines and are also able to give rise to dendritic cells in the tissues

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32
Q

What happens after monocytes and neutrophils go to the site of infection?

A

other leukocytes (e.g. eosinophils) and lymphocytes also enter the infected site

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33
Q

What is the mechanism of monocytes at/near the site of infection?

A
  1. bind adhesion molecules on vascular endothelium near site of infection & receives chemokine signal 2. migrates into surrounding tissue 3. differentiates into inflammatory monocyte at site of infection
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34
Q

What is endothelial activation? How are these changes induced?

A

changes that occur in endothelium as a result of inflammation. induced by variety of inflammatory mediators released as a consequence of recognition of pathogens by macrophages & later by neutrophils & other WBCs

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35
Q

What causes swelling & pain during infection? What else can this cause?

A

major changes in local blood vessels & increase in vascular permeability. can also cause accumulation in tissues of plasma proteins such as complement & MBL that aid in host defense

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36
Q

What are lipid mediators of inflammation?

A

secreted by macrophages & neutrophils: prostaglandins, leukotrienes, & platelet-activating factor (PAF) which are rapidly produced by enzymatic pathways that degrade membrane phospholipids

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37
Q

How are mast cells activated?

A

by C5a from the complement system

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38
Q

What do activated mast cells do?

A

stimulated to release their granules containing the small inflammatory molecule histamine, TNF alpha, and cathelicdins

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39
Q

What are the 2 protective enzymes cascades triggered by injury to blood vessels if a wound occurs?

A
  1. kinin system 2. coagulation system
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40
Q

What is the kinin system (enzyme cascade)?

A

plasma proteases that is triggered by tissue damage to generate several polypeptides that regulate blood pressure, coagulation, and pain

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41
Q

What is bardykinin?

A

inflammatory mediator vasopeptide produced by the kinin system. increases vascular permeability to promote influx of plasma proteins to the site of tissue injury -> causes pain

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42
Q

Why is pain an important immunological response?

A

draws attention to the problem & leads to immobilization of the affected part of the body which helps to limit the spread of the infection

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43
Q

What is the coagulation system (enzyme cascade)?

A

activation leads to formation of fibrin clot & prevent blood loss. in innate immunity clot physically encases infections microorgansims & prevents their entry into the bloodstream

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44
Q

What are toll like receptors (TLRs)?

A

induces the expression of several host defenses . leads to cytokine and chemokine production by macrophages. activated by different PAMPs (pathogen associated molecular patterns)

45
Q

How do TLRs exist?

A

hetero/homodimers

46
Q

How many LRRs (leucine rich repeats) do TLPs have?

A

18-25

47
Q

What do TLRs bind to?

A

product of gram negative bacteria

48
Q

What happens when PAMPs are recognized by TLR-1 and TLR-2?

A

dimerization of the TLRs and signaling: 2 TLRs bind to the same lipopeptide

49
Q

What is TLR-4 expressed by and why is it important?

A

several types of immune-system cell (dendritic cells & macrophages) & is important in sensing and responding to numerous bacterial infections

50
Q

What does TLR-4 recognize?

A

LPS of gram negative bacteria by mechanism that is part direct and part indirect (in associated with host accessory proteins MD-2 and CD14)

51
Q

What is septic shock?

A

uncontrolled systemic bacterial infection, sepsis, due to systemic injection of LPS that causes collapse of circulatory & respiratory systems

52
Q

What does LPS cause?

A

overwhelming secretion of cytokines (TNF-alpha) that causes systemic vascular permeability (undesirable effect of its normal role in containing local infections)

53
Q

What do TLRs activate? What does this induce?

A

activates: NFkB, AP-1, and IRF transcription factors induces: expression of inflammatory cytokines and type I interferons

54
Q

What do mammalian TLRs interact with? What does this induce?

A

different TIR-domain adaptor molecules to activate downstream signaling pathways. induces production of: cytokines, chemotactic factors, antimicrobial peptides, & antiviral cytokines interferon alpha and beta (IFN-alpha & beta), type I interferons

55
Q

What does transcription factor NFkB induce?

A

expression of pro-inflammatory cytokines

56
Q

What do ubiquitin K63 linkages do?

A

generates platform/scaffold

57
Q

What are the 2 ways antiviral interferons in response to viral NAs can be stimuated?

A
  1. TLR-3 bind dsRNA & signals vai TRIF 2. TLR-7 binds ssRNA & signals via MyD88: both induce IFN gene expression
58
Q

What are NLRs?

A

NOD-like receptors are intracellular sensors of bacterial infection & cellular damage. has centrally located nucleotide binding oligomerization domain (NOD) & other variable domains that detect microbial products or cellular damage or that activate signaling pathways

59
Q

What is the mechanism of intracellular NOD proteins?

A

recognize bacterial peptidoglycans and activate NFxB to induce expression of proinflamatory genes. NFxB then induces expression of genes for inflammatory cytokines & enzymes involved in production of nitric oxide (toxic to bacteria & intracellular parasites)

60
Q

Compare/contrast NLR and TLR pathways.

A

NLR is intracellular vs. TLR is extracellular but both have same outcome

61
Q

What are NLRP proteins? What do they do?

A

subfamily of NLR proteins w/ pyrin domain in place of CRD domain at amino termini. react to infection or cellular damage through inflammasome to induce cell death & inflammation

62
Q

How is NLRP3 inflammasome activated? What does it produce?

A

activated by cellular damage to produce pro-inflammatory cytokines

63
Q

What does caspase 1 activation induce?

A

cell death (pyroptosis) due to release of these pro-inflammatory cytokines upon cell rupture

64
Q

What are inflammasomes made of?

A

several filamentous protein polymers created by aggregated CARD and pyrin domains

65
Q

What do RIG-I-like receptors detect? What do they induce?

A

(retinoic acid inducible gene I) cytoplasmic viral RNAs and activate MAVs to induce type interferon production and pro-inflammaotry cytokines

66
Q

What do TLR-3, TLR-7, & TLR-9 detect?

A

extracellular viral RNAs and DNAs that enter the cell from the endocytic pathway

67
Q

How are viral RNAs produce WITHIN a cell sensed?

A

RIG-I-like receptors (RLRs): “viral sensors”

68
Q

What do cytosolic DNA sensors signal?

A

through STING (stimulation of interferon genes) to induce production of type I interferons when protozoan, viral, microbial is in the cytoplasm during infection

69
Q

What is cGAS?

A

cytosolic sensor of DNA that signals through STING to activate type I interferon production

70
Q

What are CDNs?

A

bacterial cyclic dinucleotides

71
Q

What effect other than activating effector functions and cytokine produce can activating the innate sensing pathways have?

A

induction of co-stimulatory molecules on tissue dendritic cells & macrophages: important link between innate & adaptive immune response

72
Q

What does bacterial LPS induce?

A

changes in dendritic cells, stimulating them to migrate & initiate adaptive immunity by activating T cells

73
Q

What are 2 important co-stimulatory molecules?

A
  1. B7.1 (CD80) 2. B7.2 (CD86) induced on macrophages & tissue dendritic cells
74
Q

What are B7.1 & B7.2 important?

A

recognized by co-stimulatory receptors expressed by cells of adaptive immune response (CD4 T cells) & activate them: important step in activating adaptive immune response

75
Q

What is the acute-phase response?

A

live produces proteins that act as opsonizing molecules helping to augment the action of complement

76
Q

What occurs at the site of infection during induced innate response?

A

1.production & recruitment of fresh phagocytes 2. acute phase response 3. platform of adaptive immunity

77
Q

What are the 3 kinds of cytokines?

A
  1. autocrine (self) 2. paracrine (nearby) 3. endocrine (distant)
78
Q

What are interlukins (ILs)?

A

cytokines secreted by and acting on leukocytes

79
Q

What are the 3 families of cytokines?

A
  1. IL-1 (1-11) 2. TNF 3. interferon
80
Q

What is IL-1: the hematopoietin superfamily?

A

regulates non-immune system growth & differentiation too/ IL6 is a members & so is the cytokine GM-CSF that stimulates production of new monocytes & granulocytes in bone marrow

81
Q

What is the mechanism of the JAK-STAT pathway?

A
  1. binding of JAK 2. dimerize 3. STATs bind & are phosphorylated by JAKs 4. phosphorylated STATs form dimers that translocate into nucleus to initiate gene transcription (STATs = signal transducers and activators of transcription)
82
Q

What do cytokines and chemokines do?

A

messengers released by macrophages and dendritic cells that recruit effector cells

83
Q

What are some important cytokines and chemokines?

A

IL-1beta, IL-6, CXCL8, IL-12. TNF-alpha (IL-1beta, TNF alpha, IL-6 = induce fever)

84
Q

What do cell-adhesion molecules control?

A

interactions between leukocytes & endothelial cells during inflammatory response

85
Q

What are the 3 types of cell-adhesion molecules & where are they located?

A
  1. selectins (endothelial cells) 2. integrins (neutrophils, moving cells) 3. immunoglobulin superfamily (endothelial cells)
86
Q

Who mediates phagocyte adhesion to vascular endothelium?

A

integrins: ICAM-1 and ICAM-2 are integrins expressed by phagocytes

87
Q

What is extravasation?

A

migration of leukocytes out of blood vessels in response to signals generated at sites of infection (neutrophils are 1st)

88
Q

What is the mechanisms of TNF-alpha action?

A

released systematically has local protective effects (expression of adhesion molecules & extravasation of cells such as monocytes & neutrophils) but it has catastrophic effects if released in the bloodstream

89
Q

What cytokines elevate body temperature?

A

TNF-alpha, IL-1-beta, and IL-6

90
Q

What are endogenous pyrogens?

A

TNF-alpha, IL-1-beta, and IL-6 cause fever and derive from endogenous source. synthesize prostaglandin E2 by COX-2 enzyme -> E2 then acts on hypothalamus -> increase in heat from catabolism & retention from vasoconstriction -
> decreases loss of excess heat through the skin

91
Q

What are exogenous pyrogens?

A

induce fever from bacterial components such as LPS. promote production of endogenous pyrogens & directly inducing cyclooxygenase-2 as consequence of signaling through TLR-4 leading to production of E2

92
Q

Why is a fever good?

A

most pathogens grow better at lower temps whereas adaptive immune responses are more intense at elevated temperatures

93
Q

What are eicosanoids?

A
  1. lipid mediators/local hormones 2. strong hormone like actions in tissues where they are produced 3. specific effects on target cells CLOSE to their site of formation 4. rapidly degraded -> not transported to distal sites within the body 5. not stored & very unstable
94
Q

Where are eicosanoids made?

A

all cell types except for RBCs

95
Q

What are the 3 pathways of eicosanoid biosynthesis?

A
  1. cyclooxygenase (COX) - produces prostaglandins & thromboxanes 2. lipoxygenase (LO) - produces leukotrienes, lipoxins, 12-15 HETES, and hepoxilins 3. cytochrome P450s (monooxygenases) - produce other HETEs (20-HETE), principal pathway in the proximal tubules
96
Q

Why are prostaglandins important?

A

induce fever

97
Q

What are the biological actions of eicosanoids? What occurs if they exist in excess?

A

actions: regulation of BP, blood clotting, & system modulation excess: pain, inflammation, fever, nausea, and vomiting

98
Q

What are the effects of TNF-alpha, IL-1beta, IL-6beta?

A
  1. neutrophil mobilization 2. acute phase proteins in liver 3. increased body temperature 4. protein & energy mobilization to allow increased body temperature 5. TNF alpha stimulates migration of dendritic cells to lymph nodes & maturation for initiation of adaptive immune response
99
Q

What are some acute phase proteins?

A

SAP & CRP, MBL (activate lectin pathway of complement system)

100
Q

What do interferons do?

A

interfere with viral replication

101
Q

What are type 1 interferons?

A

IFN alpha & IFN beta: made by almost all cell types (pDCs and IPCs in particular)

102
Q

What are type 2 interferons?

A

INF-gamma

103
Q

What do plasmacytoid dendritic cells (pDCs) do?

A

make abundant type I interferons: up to 1000x times more than other cell types bc of efficient coupling of viral recognition by TLRs of the pathways of interferon production

104
Q

What is true about NK cells and innate lymphoid cells?

A

have lymphoid characteristics but which lack specific antigen receptors. have same common lymphocyte progenitor (CLP) that gives rise to B and T cells. effector cells that amplify signals delivered by innate recognition

105
Q

What is adaptive immunity?

A

clonal expression of antigen receptors produced by somatic genes rearrangements that provide the extraordinarily diverse specificities of T and B lymphocytes

106
Q

How are NK cell activated?

A

type I interferon and macrophage derived cytokines

107
Q

How do NK cells kill target cells?

A

balance between activating and inhibitory signals. “stress induced self” vs “missing self” activating vs. inhibitory receptors. also through expression of TRAIL (TNF family member) which binds to TNFR of DR4 & DR5 that activates procaspase 8 leading to induction of apoptosis of the target cell

108
Q

How do viruses & pathogens use MHC class I molecules?

A

prevent display of antigens as peptides to T cells

Immunology (8 decks)

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