Immunology Exam 1 Flashcards


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1

Edward Jenner

father of immunology; studied smallpox

2

Smallpox

affected anyone and everyone; use cowpox to confer protection (unethical experiment)

3

types of pathogens (4)

bacteria, viruses, parasites, fungi

4

opportunistic pathogens

microorganisms that cause disease only when IS is compromised

5

commensal organisms

microbes that live in a healthy adult

6

Immune response

our body's response against infection

7

immunology

the study of the body's physiological defense against invading organisms

8

layers of defense of the immune system

anatomic barriers-> complement antimicrobial proteins-> innate immune cells-> adaptive immunity

9

anatomic barriers

covering membranes

ex: skin, oral mucosa

10

complement antimicrobial proteins

present right away in the blood serum; antimicrobial proteins

ex: C3, defensins, RegIIIy

11

antibicrobial proteins

epithelial surfaces immune cells (Neutrophils)

12

innate immunity

active early, limited in how many pathogens can be recognized.

Rapid response

Ex: macrophages, granulocytes, NK cells, epi cells

13

adaptive immunity

developed over time- adapts to the pathogen, highly specific, provides protective immunity- memory

Slow response

ex: B cells/antibodies, t cells

14

effector mechanism

methods to kill or destroy a pathogen.

15

effector cells

cells using effector mechanism

16

Innate immune response process

bacterial cell surface induces cleavage and activation of complement-> one complement fragment covalently bonds to the bacterium and the other attracts an effector cell-> the complement receptor on the effector cell bind to complement fragment on the bacterium-> effector cell engulfs the bacterium, kills it and breaks it down

17

Innate immune response on the skin

surface would introduces bacteria-> activates resident effector cells to secrete cytokines-> vasodilation and increase vascular permeability allow fluid protein and inflammatory cells to leave blood and enter tissue-> the infected tissue becomes inflamed, causing redness, heat, swelling and pain

18

effector cells in innate immunity functions

phagocytose bacteria

make cytokines

19

cytokines

messengers that start inflammatory response, communicators

call other immune cells in

20

adaptive immune response cell

lymphocytes- B and T cells

21

what undergoes clonal selection and clonal expansion

adaptive- lympocytes

22

clonal selection

only antigen-specific lymphocytes- proliferate and differentiate

only those w receptors for pathogen causing infection will be selected to play a role in adaptive response

23

clonal expansion

multiplication of antigen-specific lymphocytes

24

adaptive IR process

clonal selection (progenitor cell gives rise to lg number of lymphocytes each w different specificity-> removal of potentially self reactive immature lymphocytes by clonal detection-> pool of mature lymphocytes)-> clonal expansion (proliferation/ differentiation of activated lymphocytes to form a clone of effector cells)

25

naive

not yet encountered pathogen

26

primary IR

first time the adaptive IS sees a pathogen

27

secondary IR

second and all subsequent times that the adaptive IS sees a pathogen

memory cells

28

how long does it take for secondary IR to form

3-5 days

29

immunological memory

some lymphocytes persist- long term protection

30

Immune system functions (4)

1. immunological recognition

2. immune effector function

3. immune regulations- control so doesn't attack self

4. immunological memory (adaptive only)

31

Cells of the immune system

leukocytes (WBC)

32

where do leukocytes originate

bone marrow

33

hematopoiesis

development of blood cells

34

three blood cell lineages

lymphoid, myeloid, erythroid

35

HSC

hematopoietic stem cell

self renew, mulipotent

give rise to lymphoid, myeloid and erythroid lineages

36

multipotent

Multiple potential of what they'll become

37

lymphoid lineage development

HSC (bone marrow)-> common lymphoid progenitor (bone marrow)-> B cell, T cell, NK cell, ILC (blood-> lymphoid tissues-> effector cells)

38

myeloid lineage development

HSC-> common myeloid progenitor-> granulocyte/macrophage progenitor and megakaryocyte/erythrocyte progenitor OR immature DC-> mature DC OR granulocytes then immature DCs and mast cell macrophages

39

erythroid lineage development

HSC-> common myeloid progenitor-> megakaryocyte/erythrocyte progenitor-> megakaryocyte and erythroblast-> platelets (from megakaryocytes) and erythrocyte (from erythroblast)

40

major innate cells

myeloid lineage

granulocytese, macrophages, Dendritic cells, mast cells

41

granulocytes

prominent cytoplasmic granules, single lobed nucleus

neutrophils, eosinophils, basophils

42

neutrophils

most abundant

phagocytose and kill pathogens and activate bacterial mechanisms

43

eosinophils

2nd most abundant

defense of parasite and allergens- kill Ab coated parasites

44

basophils

least abundant

defense against parasite/ allergic responses

45

macrophage

phagocytosis/bacterial mechanism activation

antigen presentation/ cytokine production

innate but start to inform adaptive

46

dendritic cells

antigen uptake

antigen presentation/ cytokine production

resident in body tissues

47

mast cells

release of granules containing histamine and active agents

resident in CT

48

the link between innate and adaptive immunity

dendritic ce;;s

49

mature dendritic cells

migrates through bloodstream, enters tissues

undergoes macropinocytosis

50

macropinocytosis

process of ingesting lg amounts of ECF from environment and look for pathogen

51

Dendritic cells when they encounter a pathogen

mature- able to activate T cells

52

antigen presenting cells

DCs also called

53

DC process

reside in peripheral tissues and encounter pathogen-> DCs migrate via lymphatic vessels to regional LNs and mature-> mature DCs activate naive T cells in lymphoid organs

54

name of T cells after encountering pathogen

activated T cells

55

lymphoid lineage is a part of what IR

adaptive (mostly)

56

what cell is in the lymphoid lineage but innate

NK cells

57

Natural Killer Cells

not antigen-specific

active against tumor cells and virus infected cells

58

lymphocytes

antigen specific

1 billion constantly circulating

without infection- small and featurelist

59

lymphoid lineage maturation

common lymphoid progenitor-> B cell-> lymph node B cells-> effector cells- plasma cells

common lymphoid progenitor-> T cell-> lymph node T cells-> effector cells- activated T cell

common lymphoid progenitor-> NK cell-> lymph node NK cell-> effector cells- activated NK cell

60

B lymphocytes undergo what type of immunity

humoral

61

humoral immunity

fluid-phase immunity

62

immunoglobulin

cell-surface receptor for pathogen- held at surface very early then secreted

63

B cell effector cell

plasma cell

64

plasma cell

secrete soluble Igs or antibodies "Ab factories"

65

How do Abs fight pathogens

neutralization and opsonization

66

neutralization

blocking a toxin

67

opsonization

coat surface of bacteria with Abs-> easily recognized by IS

68

how many Abs can each lymphocyte recognize

one

69

what type of immunity does T lymphocytes have

cell-mediated immunity

70

cell-mediated immunity

cell contact with the pathogen

71

T-cell receptor (TCR)

cell-surface receptor for pathogen

never secreted- always receptor

72

T lymphocytes effector cells

cytotoxic, helper, or regulatory T cells

73

cytotoxic T cells

killer T cells

74

helper T cells

make cytokines; help activate killer T and B cells

75

regulatory T cells

help dampen IR-> balance response and controls

76

How Abs Combat Infections

specific Ab-> bacterial toxins-> neutralizations-> ingestion by macrophage

specific Ab-> bacteria in extracellular space-> opsonization-> ingestion by macrophage

specific Ab-> bacteria in plasma-> complement activation-> lysis and ingestion

77

complement system

series of serum proteins

78

complement system function

ingestion bc complements coats bacteria and make it more recognizable

79

lymphoid organs

aggregates of lymphocytes in a framework of non-lymphocytes

80

central (primary) lymphoid organs function

lymphocyte generation-> where lymphocytes are made

81

Central (primary) lymphoid organs

bone marrow and thymus

82

where are B cells made

in the bone marrow

83

where are T cells made

thymus

84

peripheral (secondary) lymphoid organ functions

naive mature lymphocyte maintenance; adaptive IR initiated

85

peripheral (secondary) lymphoid organs

lymph nodes, spleen, MALT (gut, nasal, respiratory, and urogenital)

86

MALT stands for

mucosal-associated lymphoid tissue

87

lymphocyte recirculation

small lymphocytes move bw the blood and lymph

lymphocytes continually survey secondary lymphoid organs

88

what if there is infection found while lymphocytes are surveying?

stay and start to develop response

89

where do lymphocytes meet pathogens

in draining lymph nodes; DCs bring pathogens or components of pathogens to the draining LNs

lymphocytes activated by pathogen in LN-> stay

90

how do naive lymphocytes arrive at LNs

in arterial blood

91

how do pathogens reach LNs from site of infection

via afferent lymphatic vessels w/ cytoskeletal changes

92

process of circulation of lymphocytes

naive lymphocytes arrive to LNs in arterial blood and pathogens via lymphatics ->draining LNs-> lymphocytes and lymph return to the blood via lymphocytes-> venous blood-> venous blood returns to the heart-> L subclavian vein

93

paracortical area of the LN contains

mostly T cells

94

LN T cell areas are activated by

DCs

95

LN B cell areas

B cells to lymphoid follicles if bind to pathogen-> expand-> reproduction, tons of very specific B cells

96

three phases of the immune response

innate phase, induced innate response, adaptive phase

97

innate phase goal

to kill or weaken pathogen

98

parts of the innate phase

antimicrobial enzymes, antimicrobial peptides, complement system

99

antimicrobial enzymes function

digest bacterial cell walls

100

antimicrobial peptides function

lyse bacterial cell membranes directly

101

complement system function

targets pathogens for lysis and phagocytosis

102

induced innate response includes

PAMP recognition, cellular actiation

103

PAMP stands for

pathogen-associated molecular patterns

104

cellular activation is

inflammation

105

adaptive immune response includes

Antigen-specific lymphocytes, memory response

106

Process of the Immune Response

pathogen-> containment by an anatomic barrier-> if fails->

Innate phase: infection-> recognition by preformed, nonspecific and broadly specific effectors-> if fails->

Induced Innate response: recruitment of effector cells-> recognition of PAMPs, activation of effector cells and inflammation-> if fails->

adaptive immune response: transport of antigen to lymphoid organs-> recognition by naive B and T cells-> clonal expansion and differentiation to effector cells-> removal of infectious agents

107

stages of infection and body's response to

pathogens adhere to epithelium (normal flora, local chemical factors, phagocytes)

-> local infection, penetration of epithelium (wound healing induced, antimicrobial proteins and peptides, phagocytes and complement destroy invading microorganisms->

local infection of tissues (complement, cytokines, chemokines, phagocytes, NK cells; activation of macrophages; DCs migrate to LNs to initiate adaptive; blood clotting helps limit spread of infection)->

adaptive immunity

108

where can pathogens be found during infection

extracellular and intracellular

109

extracellular pathogens

most have extracellular component; bacteria, viruses, fungi, parasites

110

effector response to extracellular pathogens

soluble/secrete molecule-> many promote phagocytosis

111

where can extracellular pathogens be found

interstital spaces, blood, lymph, epithelial

112

protective immunity against extracellular pathogens

interstitial spaces, blood, lymph: complement, phagocytosis, Abs

epithelial: antimicrobial peptides, Abs

113

intracellular pathogens

some bacteria, viruses

114

effector response to intracellular pathogens

kill infected cells-> epose to the soluble/secreted molecules

115

Protective immunity against intracellular pathogens

cytoplasmic: NK cells, cytotoxic T cells

Vesicular: T-dependent and NK cell-dependent macrophage activation

116

how do pathogens damage body tissues

direct: exotoxin production, endotoxin, direct cytopathic effect

indirect: immune complexes, anti-host Ab, cell-mediated immunity

117

exotoxin production

released by pathogen and act at the surface of host cell; bind to our cell receptors

direct mechanism

118

endotoxin

part of microbial structure activate phagocytes-> release cytokines-> local and systemic response

direct mechanism

119

direct cytopathic effect

direct damage to infected cell

120

immune complexes

Ag:Ab complexes-> further activate IR-> tissue damage

121

anti-host Ab

Ab that cross react with host cells

indirect mechanism of tissue damage by pathogens

122

cross react def.

recognize the pathogen and our cell thats similar to

indirect mechanism of tissue damage by pathogens

123

cell-mediated immunity damage to tissues

T cells that kill infected cells

indirect mechanism of tissue damage by pathogens

124

Epithelial cell barrier in skin, gut, lungs, eyes/nose/oral cavity

skin: stratified epi

gut: single cell layer of columnar epi

lungs: upper airway- pseudostratified columnar; lower airway- single cell layer of columnar epi

eyes/nose/oral cavity: pseudostratified columnar

125

epithelial cells are joined by

tight junctions

126

mechanical protection of skin, gut, lungs, eyes/nose/oral cavity

skin/guts: longitudinal flow of air or fluid

lungs: movement of mucus by cilia

eyes/nose/oral cavity: tears, nasal cilia

127

chemical protection of skin

beta defensins

128

chemical protection of gut

alpha defensins

129

chemical protection of lungs

alpha defensins

130

chemical protection of eyes/nose/oral cavity

beta defensins

131

microbiological protection of skin, gut, lungs, eyes/nose/oral cavity

normal microbiota

132

antimicrobial peptides molecule type

soluble effector molecules

133

antimicrobial peptides are made by

mammals, insects and plants

134

antimicrobial peptide function

constantly secrete at mucosal surfaces

135

largest family of antimicrobial peptides

defensins

136

defensins activity

minutes to disrupt cell membrane of bacteria, fungi and envelopes of some viruses

137

defensin structure

cationic peptides (35-40 AAs)- positively charged peptides-> how bacteria is effected

amphipathic structure- pos and neg parts

138

propeptides

much bigger-> get processed down to smaller

139

what type of processing of antimicrobial peptides

proteolytic processing from propeptides

140

subfamilies of defensins

alpha, beta, sigma

141

alpha defensins are stored in

in primary granules of neutrophils

142

alpha defensins are made by

paneth cells of gut

143

beta defensins are made and stored by

epithelia of skin, respiratory, and urogenital tracts

144

sigma defensins

little to know, inactive to humans

145

how do defensins get into the bilipid layer and what do they form?

electrostatic attraction and the transmemrane EF bring the defensin into the bilipid layer and form a pore

146

the complement system

system of plasma proteins, series of enzymatic reactions

147

plasma proteins are made by?

constitutively made by the liver

148

plasma proteins are found where?

in blood, lymph, ECF

149

the complement system targets pathogens for

direct pathogen lysis, phagocytosis, inflammation

150

jules Bordet

discovered the complement of serum that complements the action of Abs

151

complement system overall process

1. pattern-recognition

2. protease cascade

3. targets pathogens

152

different pathways of the complement system

lectin, classical, alternative

all lead to C3 convertase-> phagocytosis, C3b engulfs and destroys pathogen, and formation of MAC

153

what do the complement system pathways use

zymogens

154

zymogens

inactive form of protease; requires cleavage by another protease to become acive

155

Complement activation results in _________ attachment of _____ to the pathogen's surface

covalent, C3b

156

C3 is cleaved into

C3a and C3b

157

C3a

anaphylotoxin

158

anaphylotoxin

chemicals that help recruit phagocytes, make vessels more leaky to allow over and communicate to go

can induce anaohylactic shock

159

C3b

opsonizes pathogen, provides for next stems in the pathway=critical

160

complement fixation

covalent attachment of C3b (or C4b) to pathogen surface

161

what problem do people have if they lack C3

have recurrent infections

162

How does C3b get attached to the pathogen surface

before cleavage by C3 convertase, thioester bond is protected from reacting-> cleavage of C3 releases Ca and C3b with conformational change that allows thioester bond to react with chemical group on pathogen surface making C3b bound

163

what happens to the C3b if there is no pathogen

C3b thioester bond inactivated by hydrolysis

164

yeast in lectin pathway

microorganisms-> repeating molecular structures-> PAMPs

contain many mannose residues

165

PAMPs

pathogen associated molecular patterns

166

vertebrates in lectin pathway

carb side chain has sialic acid residues-> lectin pathway will not bind/recognize

167

mannose-binding lectin (MBL) are what type of lectin

C-type lectin

168

C-type lectin

group of carb binding proteins; require calcium

169

what do mannose binding lectin bind to

mannose containing carbs of pathogen

170

effects of mannose binding lectin binding to pathogen surface

1. acts as opsonin- more recognized

2. Triggers lectin pathway- complement activation

171

MBL monomers form

trimeric clusters of carb recognition domains by binding with high acidity to mannose and fructose residues

172

avidity

total high binding strength

173

Lectin Pathway

MBL + MASP1 + MASP2 (all inactive)-> bind to pathogen surface-> conformational change (MASP1)-> activate MASP2-> C4-> Ca and C4b (C4b bound to pathogen surface)-> C4b binds to C2-> MASP2 cleaves into C2b(released) and C2a-> C4b2a (C3 convertase)-> C3 (active)-> cleaved into C3a and C3b

174

C3a function

inflammation response

175

C3b function

bind pathogen surface

176

classical pathway goal

eventual generation of classical C3 convertase

177

Classical pathway contains the

C1 complex- binds to either CRP or Ab-> can recognize

178

CRP

C-reactive protein- can bind to the pathogen surface

179

Classical Pathway Process

C1 complex (C1q, C1s, C1r)-> attach to pathogen surface (C1q is the attachment pt)-> C1r:C1s conformational change-> C1r becomes active-> C1s becomes active-> C1s cleaves C4 (active)-> C4a and C4b-> C4b binds to microbial surface -> binds C2-> C1s cleaves C2 into C2b and C2a-> forms C4b2a (C3 convertase)-> cleaves C3 into C3a and C3b

180

alternative pathway process

C3b (pathogen surface)-> bind factor B-> conformational change-> factor D cleaves into Ba (released) and Bb (still bound to C3b)-> C3bBb (alternative C3 convertase)

181

alternative pathway spontaneous activation of C3

C3 (H20)-> binds to factor B-> Ba and Bb-> C3(H2O)Bb

182

fluid phase C3 convertase

C3(H2O)Bb

183

C3 convertase

C4b2a

184

alternative C3 convertase

C3bBb

185

once activated, how does complement have its effects?

generate C3 convertase which cleaves C3 leaving C3b bound to microbial surface and releasing C3a-> inflammatory cells recruited, opsonization-> perforation of pathogen surface

186

inflammatory cell recruitment

C3a and C5a recruit phagocytic cells to site of infection and promote inflammation

187

Opsonization in complement

C3b coats to make more recognizable, phagocytes with receptors for C3b enguld and destroy the pathogen

188

perforation of pathogen membrane

generate C5 convertase that leads to formation of membrane-attack complex (MAC)-> disrupts cell membranes

189

receptors for anaphylotoxins

on phagocytes, endothelial cells, mast cells

190

anaphylatoxins act on

BVs to increase vascular permeability and cell adhesion molecules

191

anaphylatoxins acting on BVs result in

increased permeability- leakage of fluid and complement from BVs-> provide more fuel for response

migration of macrophages, neutrophils and lymphocytes-> increase in microbial activity-> very active when they get there-> combat

192

pathogen opsonization process

CR1-complement receptor 1= bind to C3b-> helps recognize, bring in + destroy

bacterium coated in C3b-> only C3b binds to CR1, bacteria not phagocytosed-> C5a can activate macrophages to phagocytose via CR1

193

perforation of pathogen cell membrane C5 process

C3b binds C4b2a and C3bBb-> form C5 convertases (C4b2a3b or C3b2Bb)-> C5 cleaved by active C2a or active Bb-> C5a released and C5b

194

C5b

initiate terminal complement complex

195

MAC causes

loss of cellular homeostasis

disrupt proton gradient

enzymes (lysozymes) enter pathogen

196

perforation of pathogen cell membrane C6-C9 process

C5b-> bind to C6 (C5b6)-> bind to C7 (C5b67) insert in lipid bilayer-> bind to C8 (C5b678)-> bind to C9 (polymerization of 10-18 C9)-> MAC

197

regulation in the alternative pathway

properdine (+)

CR1 (-)

DAF (-)

Factor H (-)

198

properdine regulation

stabilize Bb (+)

199

CR1 regulation

binds C3b or C4b, displace Bb (-)

200

DAF regulation

competes with factor B, displaces Bb (-)

201

Factor H

bind C3b, displace Bb

202

Lectin pathway regulation

CR1

203

C3 Convertase regulation

Factor I (-)

CD59/protectin (-)

204

factor I regulation

cleaves C3b-> inactive (-)

205

CD59/protectin

binds to C8-> prevents C9 recruitment

prevents final complex (-)

206

enzyme linked Immunosorbent assay (ELISA)

direct binding assay for ag or ab, enzyme chemically linked to ab, purpose: quantify how much ag in sample

207

ELISA steps

protein of interest bound to well

blocking-coat rest of plate

abs- primary, secondary...

substrate added-color change

Data-> standard curve

208

direct ELISA process

ag-> block-> primary w enzyme

209

indirect ELISA process

ag-> block-> primary Ab (acts as bridge)-> secondary Ab w enzyme

210

capture/sandwich ELISA process

Ab complement-> ag-> ab

211

primary Ab

complementary to/ binds ag

212

secondary ab

binds primary ab

213

immunofluorescense

using fluoroflor; must use microscope

214

immunohistochemistry

tissue is fixed depositing color in T cell; light microscope

215

immunofluorescence purpose

look at location of proteins in tissues

216

direct immunofluorescence

ab gets attached to Ag directly

217

indirect immunofluorescence

ab of one species bound to ag and ab of other species bound to that one

218

immunofluorescence data

images- can be quantified

219

flow cytometry purpose

define (size, granularity,protein expression), enumerate populations of cells/collect cells; cell sorting

220

flow cytometry general procedure

generate single cell suspension

cells stained with Fluorescence-Abs

cells move by the laser (single-file)

emitted light detected by optical system

computer analysis

221

gating

selection of subpopulations for analysis

222

data analysis marker correlation

marker on y-axis=marker 2; marker on x-axis= marker 1

upper left: marker 2 pos.

upper right both pos

lower left both negative

lower right marker 1 pos

223

advantages of data analysis

single cell analysis from complex sample

high-throughput

very specific for rare cell populations

isolation of cells with very high purity

224

disadvantages for data analysis

need single cell suspension

limited to less than 20 parameters

technique is not standart

subjective nature

225

PRPs stands for

pathogen recognition receptors

226

PRPs

free receptors, membrane bound phagocytic and signaling receptors, cytoplasmic signaling receptors

227

cell surface receptor function

distinguish self from nonself

228

cell surface receptor: macrophages

recognize the cell surface carbs of bacterial cells but not those of human cells

229

cell surface receptor: NK cells

recognize changes at the surface of human cells that are caused by viral infection

230

DCs are generated from

myeloid and lymphoid progenitors

231

types of immature DCs

cDC and pDC

232

cDC

conventional, classical DC

233

cDC

resident in tissue, pick up pathogen and take back to LN

234

pDC

plasmacytoid, extremely good at viral responses

235

phagocytic receptors recognize

carbs and lipids

236

phagocytic receptor function

bind to pathogen-> phagocytose pathogen-> phagolysome (destroy)-> phagosome formed with lysosome

237

C-type lectins recognize? Target?

recognize carbs on surface of pathogens; target bacteria and fungi

238

ctype lectins ligand

beta glucans (fungi), mycobacterial ligand (bacteria)

239

scavenger receptors recognize

bacteria

240

scavenger receptors ligands

LPS, LTA, proteins, CpG DNA

241

scavenger receptors look for

damaged, low density lipoprotein

242

complement receptors targeting

bacteria/fungi

243

complement receptor ligands

beta glucans(fungi), oligosaccharides and proteins (bacteria)

244

receptor mediated endocytosis process

macrophage receptors that recognize complements of microbial surfaces-> microorganisms bound by phagocytic receptors on the macrophage surface-> microorganisms internalized by receptor-mediated endocytosis-> fusion of the endosome with a lysosome forms a phagolysosome in which microorganisms are degraded

245

bactericidal

kill

246

bacteriostatic

slow down

247

toll-like receptors

intracellular or on surface response to form cytokines- some endosomal that recognize nucleic acids

248

TLR ligands

carbs, lipids, proteins, nuceic acids

249

TLR process

1. recognize

2. signaling to nucleus

3. gene expression (cytokines)-> bring more immune cells in

250

TLR embryonic development:

controls dorso-ventral gene patterning

251

TLR adult

controls host defense agains gram pos bacteria and fungus

252

LRR

leucine rich repeat region, recognition domain, horse-shoe shape

253

TIR

toll interleukin/receptor domain, signaling

254

dimer formed

heterodimer if TLR2 is involved, rest are homodimers

255

MyD88 dependent TLR signaling

all except TLR3

256

MyD88 dependent process

recognition: TLR dimer forms

MyD88 recruited/scaffold

IRAKs recruited

TRAF6 recruited and activated-> polyubiquitinated

Kinases activated- moce phosphates

IkB phosphorylated and degraded- inhibits NFkB

TF (NFkB) phosphorylated and degraded

257

MyD88 independent differences from dependent

no MyD88- use TRIF

phosphorylation/polyubiquitination steps

TF (IRF3)- interferon regulatory factor

258

viruses use host cell for

transcription, translation, replication,

259

what are viral nucleic acids detected by

endosomal TLRs- leads to type 1 interferons

260

RIG1 like receptors

contain RNA helicase like domain and 2 amino terminal CARD domains

261

helicase domain

recognition, bind to RNA

262

CARD domain

interact with adaptor proteins to activate signaling pathways

263

RIG 1

recognizes the unmodified 5' triphosphate end of ssRNA

264

MDA-5

senses dsRNA

265

RLRs

recognize viral nucleic acids; results/leads to production of type 1 interferon

266

NOD-like receptors location

cytoplasm

267

NOD like receptors function

sense intracellular pathogens and products from intracellular degradation of phagocytosed pathogens

268

NOD like receptors structural domains

NOD

LRR
CARD

269

NOD domain

helps oligomerization

270

NOD like receptors activate

NFkB-> nucleus-> gene expression