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MM Test 2 > B6.026 Autoimmunity > Flashcards

B6.026 Autoimmunity Flashcards

1
Q

what is an allergen

A

antigen that is harmless and normal in the environment is perceived as abnormal
exposure causes a robust abnormal immune response

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2
Q

how are allergies mediated

A

IgE mechanisms

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3
Q

autoantigen

A

normal part of the body (protein, DNA or RNA) that is recognized by the immune system as abnormal leading to immune activation causing destruction and inflammation or activation of an organ

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4
Q

“allo”

A

non self antigen from members of the same species

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5
Q

examples of allo antigens

A

2 major: blood group antigens and histocompatibility antigens
highly polymorphic genes

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6
Q

alloimmunity

A

occurs when the body produces antibody against the new alloantigen to which it has been exposed

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7
Q

some features of innate immunity

A
  1. accumulation and activation of leukocytes and plasma proteins at site of infection
  2. prevents organisms from getting across barriers (mucous layer, epithelium)
  3. induces inflammation
  4. defends against intracellular (viral) infected cells
  5. kill extracellular microbes
  6. recognizing microbial structures to clear dead or injured cells
  7. germ line encoded
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8
Q

some features of adaptive immunity

A
  1. combats microbes via secretion of Abs from B cells that bind to microbes, block infection of host cells, and promote phagocytosis induced destruction
  2. helper T cells recruit leukocytes to elicit microbial destruction
  3. cytotoxic T cells kill microbial infected cells
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9
Q

time frame of innate immunity

A

0-12 hours primarily

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10
Q

time frame of adaptive immunity

A

1 day and forward

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11
Q

specificity of innate immunity

A

for structures shared by classes (PAMPs) or damaged cells (DAMPs)

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12
Q

receptors of innate immunity

A

encoded in germline
limited diversity
pattern recognition receptors

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13
Q

distribution of innate immunity receptors

A

nonclonal: identical receptors on all cells of the same lineage

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14
Q

discrimination of normal self and nonself in innate immunity

A

yes

healthy host cells are not recognized, or they may express molecules that prevent innate immune reactions

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15
Q

specificity of adaptive immunity

A

for structural detail of microbial molecules (antigens); may recognize nonmicrobial antigens

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16
Q

receptors of adaptive immunity

A

encoded by genes produced by somatic recombination of gene segments; greater diversity

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17
Q

distribution of adaptive immunity receptors

A

clonal: clones of lymphocytes with distinct specificities express different receptors

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18
Q

discrimination of normal self and nonself in adaptive immunity

A

yes

based on selection against self-reactive lymphocytes; may be imperfect (giving rise to autoimmunity)

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19
Q

microbial recognition in innate immunity

A

recognize structures shared by classes of microbes not present on host cells
enhanced function through the adaptive immune system

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20
Q

microbial recognition in adaptive immunity

A

lymphocytes express receptors (antibodies) on their cell surface that recognize specific antigens
utilize cells of innate immunity to eliminate microbes
antibody (adaptive) binds to a microbe, which activates phagocytes (innate) to ingest and destroy the microbe

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21
Q

cellular compartments with receptors on innate cells

A

cell surface to detect extracellular microbes
vesicles where microbes are ingested
cytosol to sense cytoplasmic microbes

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22
Q

what are PAMPs

A

pathogen associated molecular patterns

  • microbial molecules, shared by microbes of the same type
  • not on normal host cells
  • stimulate innate immune response
  • essential for survival/infectivity
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23
Q

examples of PAMPs

A

LPS- gram neg
peptidoglycans - bacteria
terminal mannose residues - opportunistic infections
unmethylated CG-rich DNA -intracellular viral infection

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24
Q

what are DAMPs

A

damage associated molecular patterns

  • released from damaged or necrotic host cells
  • present in injury (infarction) or infection
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25
Q

PRRs

A

pattern recognition receptors
innate immune receptors that recognize PAMPs and DAMPs
toll-like receptors
nod-like receptors

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26
Q

toll like receptors (TLRs)

A

specific for microbial components

activate transcription factors to stimulate expression of genes encoding cytokines, enzyme, and other proteins

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27
Q

TLR signaling process

A
  1. TLR engages and recruits protein
  2. proteins activate transcription factors (NFKP and IRFs)
  3. increased expression of: cytokines, adhesion molecules, co-stimulators (generating inflammation)
  4. production of type 1 interferon, antiviral activity
  5. stimulates adaptive immunity
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28
Q

nod like receptors (NLRs)

A

family of cytosolic receptors that sense DAMPs and PAMPs in the cytoplasm

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29
Q

NOD-1 and NOD-2

A

contain N-terminal CARD (caspase related domains)
bacterial peptidoglycans in the cell wall
activates NF-kB

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30
Q

NLRP-3

A

recognizes microbial products, substances associated with cell damage, and endogenous substances in cells in large quantities (crystals)
enhances production of IL-1B

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31
Q

describe the inflammasome

A
  1. NLRP-3 oligomerizes with inactive form of caspase-1
  2. activation of inflammasome
  3. active caspase-1 cleaves pro-IL-1B
  4. activates IL-1B generates fever
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32
Q

inflammasome dysregulation associated conditions

A

gout- urate crystal deposit

auto inflammatory syndromes (familial periodic fear syndromes)

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33
Q

process of leukocyte recruitment

A
  1. rolling
  2. integrin activation by chemokines
  3. stable adhesion
  4. migration through endothelium (diapedesis)
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34
Q

characterize neutrophils

A

most abundant leukocyte in the blood
increase in number rapidly during infection
first cell to respond to infection (bacterial and fungal)
dominant cell of inflammation

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35
Q

function of neutrophils

A

phagocytose microbes in the blood and in tissues and destroy them through the oxidative burst
recruited to tissues to remove debris

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36
Q

lifespan of neutrophils

A

live for only a few hours

dead ones form pus

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37
Q

characterize monocytes/macrophages

A

found in all connective tissue and organs

prolonged survival in tissues

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38
Q

function of macrophages

A

activated by PRRs (TLR and NLR)
cytokine production regulates and induces inflammation
phagocytose microbes because of recognition of cell surface receptors
clear dead tissue
initiate tissue repair

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39
Q

classical macrophage activation

A 
immune signals
-TLRs
-cytokine INFy from innate and adaptive immunity
produces M1 activated macrophages
destroy microbes and induce inflammation
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40
Q

alternative macrophage activation

A

cytokines IL-4 and IL-13 (same as associated w allergies)
produces M2 activated macrophages
tissue repair and termination of inflammation (downregulate immune system)

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41
Q

dendritic cells

A

APCs
initiation production of cytokines, and thus initiate inflammation
bridge innate and adaptive immunity
-stimulate adaptive immune responses

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42
Q

characterize mast cells

A

abundant cytoplasmic and vasoactive granules

located on skin and mucosal epithelium

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43
Q

how are mast cells activated

A

microbial products binding to TLRs (innate)

antibody dependent- typically IgE mediated type 1 hypersensitivity reactions

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44
Q

function of mast cells

A

vasoactive amines (histamine and tryptase)
-increased capillary permeability
-kill bacteria and inactivate microbial toxins
synthesize and secrete lipid mediators and cytokines
-stimulate inflammation

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45
Q

NK cell markers

A

CD16+/56+

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46
Q

primary function of NK cells

A

identify infected and stressed cells and kill them

  • empty cytoplasmic granules into the extracellular space near the infected cell
  • granules enter the cell and activate enzymes to induce apoptosis
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47
Q

other uses of NK cells

A

fight intracellular microbial infections

secrete IFN-y for macrophage activation

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48
Q

how are NK cells activated

A

by macrophages and dendritic cells
IL-15: development and maturation of NK cells
IL-12 and IFN type 1: enhance NK cell killing function

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49
Q

inhibition of NK cells

A

block signaling by receptor activation specific for self MHC 1 molecules to protect healthy cells via ITIMs

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50
Q

function of ITAMs

A

eliminate cells infected with intracellular microbes via antibody dependent cellular cytotoxicity (ADCC)

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51
Q

alternative complement pathway

A

triggered when activated complement proteins on microbial surfaces are uncontrolled due to lack of regulatory proteins
innate immunity

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52
Q

classical complement pathway

A

triggered by antibodies bound to microbes/antigens

adaptive immunity

53
Q

lectin pathway

A

mannose binding lectin binds to terminal mannose residues

innate immunity

54
Q

function of activated complement proteins

A
  1. opsonization and phagocytosis (C3b)
  2. inflammation (C5a, C3a)
  3. MAC cell lysis
55
Q

plasma proteins of innate immunity

A

increase rapidly with infection = acute phase response

  • collectins
  • CRP
56
Q

collectins

A

mannose binding lectin (MBL)
-recognizes microbial carbohydrates, coating them for phagocytosis
-activation of complement by the lectin pathway
surfactant
-protects lung from infective microbes

57
Q

CRP

A

binds phosphorylcholine on microbes, opsonizes them for phagocytosis by macrophages
activates classic complement pathway proteins
non specific marker of inflammation

58
Q

what are interleukins

A

soluble proteins that cause cell signaling to generate immune and inflammatory reactions - stimulated by infection
communication between cells

59
Q

cytokines that stimulate APR protein synthesis from the liver (CPR and fibrinogen)

A

IL-6

60
Q

cytokines for recruitment of neutrophils and monocytes

A

TNF
IL-1
chemokines

61
Q

cytokines that cause fever by acting on the hypothalamus

A

TNF

IL-1

62
Q

source of TNF

A

macrophages
T cells
mast cells

63
Q

effects of TNF

A 
endothelial cell activation
neutrophil activation
fever
synthesis of APR in liver
catabolism of fat and muscle
apoptosis
64
Q

source of IL-1

A 
macrophages
dendritic cells
endothelial cells
some epithelial cells
mast cells
65
Q

effects of IL-1

A

endothelial cell activation
fever
synthesis of APR in liver
TH17 differentiation

66
Q

source of chemokines

A 
macrophages
dendritic cells
endothelial cells
T lymphocytes
fibroblasts
platelets
67
Q

effects of chemokines

A

leukocytes: increased integrin affinity, chemotaxis, and activation

68
Q

source of IL-12

A

dendritic cells

macrophages

69
Q

effects if IL-12

A

INFy production and increased cytotoxic activity of T cells and NK cells
Th1 differentiation

70
Q

source of IFN-y

A

NK cells

T lymphocytes

71
Q

effects of IFN-y

A

activation of macrophages

stimulation of some Ab response

72
Q

source of type 1 IFNs (a and B)

A

IFNa: dendritic cells, macrophages
IFNB: fibroblasts

73
Q

effects of type 1 IFNs

A

antiviral state
increased MHC 1 expression
NK cell activation

74
Q

source of IL-10

A

macrophages
dendritic cells
T cells

75
Q

effects of IL-10

A

acts on dendritic cells and macrophages
inhibition of cytokine and chemokine production
reduced expression of co-stimulators and MHC 2 molecules

76
Q

source of IL-6

A

macrophages
endothelial cells
T cells

77
Q

effects of IL-6

A

synthesis of acute phase proteins in liver

proliferation of Ab producing B cells

78
Q

source of IL-15

A

macrophages

79
Q

effects of IL-15

A

proliferation of NK and T cells

80
Q

source of IL-18

A

macrophages

81
Q

effects of IL-18

A

IFNy synthesis in NK and T cells

82
Q

source of TGF-B

A

many cell types

83
Q

effects of TGF-B

A

inhibition of inflammation

differentiation of Th17 and Treg cells

84
Q

how do innate immune cells discriminate against self antigens

A

receptors are specific for PAMPs and DAMPs, not for healthy substances
PRRs that recognize nucleic acids (present on normal cells) but they are located in cellular compartments where healthy cells are not accessible
normal mammalian cells express regulatory (protective) molecules

85
Q

how do adaptive immune cells discriminate against self antigen

A

lymphocytes that recognize self undergo apoptosis or are inactivated when they encounter self antigen

86
Q

primary function of B lymphocytes

A

neutralization of microbe, phagocytosis, and complement activation
VIA production of antibodies (IgD,A,M,G,E)

87
Q

membrane bound antibodies

A

function as B cell receptor

88
Q

which Ig is secreted onto mucosa

A

IgA

89
Q

which Igs are present on naïve B cells

A

IgM and IgD

not as important for response to antigens

90
Q

most abundant Ab in plasma

A

IgG

91
Q

which Ig crosses the placenta

A

IgG

92
Q

plasma cells

A

long living mature B cells

produce high affinity antibodies even after antigen removal in response to vaccines and infections

93
Q

memory B cells

A

long living mature B cells
do not produce Ab
rapidly respond with antigen re-exposure

94
Q

T cell dependent B cell response

A 
protein antigens cause weak or absent Ab responses without T cell help
APCs present to T lymphocytes that activate B cells to induce class switching and affinity maturation
95
Q

T cell independent B cell response

A

polysaccharides, lipids, and other non protein antigens elicit Ab production without involvement of T cells
low affinity, short lived

96
Q

primary antibody response

A

within days
IgM produced/wanes
low affinity
plasma cells go on to produce IgG long term

97
Q

secondary antibody response

A

within days
larger response
IgG
higher affinity

98
Q

describe B cell receptor signaling via complement receptors

A

B cells express complement receptor for activation when exposed to a microbial antigen
-microbial bound C3d (released from C3 during complement activation) binds to complement receptor 2 (CR2) on the B cell surface to activate B cells
C3d-CR2 binding enhances B cell activation as a part of the innate immune response

99
Q

describe B cell receptor signaling via TLRs

A

promote B cell proliferation, differentiation, and antibody secretion

100
Q

intracellular portion of BCR signaling

A
  1. Ab is bound to Ag
  2. tyrosine phosphorylation occurs
  3. activation of downstream enzymes via biochemical intermediates
  4. production of transcription factors leading to the immune response and inflammation (Myc, NFAT, NFKB, AP-1)
101
Q

positive selection

A

selects for cells that express a BCR

102
Q

negative selection

A

selects against cells with a BCR that binds self antigen with high affinity
-undergoes BCR editing or clonal deletion if self reactive

103
Q

hypersensitivity type and test mnemonic

A
  1. A
  2. C
  3. I
  4. D
104
Q

what is the general definition of hypersensitivity

A

injurious or pathologic immune reactions

exaggerated and abnormal reactions

105
Q

2 mechanisms of hypersensitivity

A
  1. an immune response to a microbe or environmental allergy causes tissue injury due to repeated or poorly controlled reactions
  2. failure of self tolerance when an immune response is generated to self (autologous) antigens = autoimmunity
106
Q

4 types of hypersensitivity

A
  1. immediate mediated by IgE binding to mast cells
  2. Ab (non IgE) mediated cell or tissue destruction
  3. Ab/Ag complex deposition causing inflammation and tissue injury
  4. T cell mediated
107
Q

describe type 1 hypersensitivity

A

true allergy or atopy

IgE antibody-mast cell mediated in response to an antigen

108
Q

examples of type 1 hypersens

A 
allergic rhinitis/conjunctivitis
food/med allergies
asthma
anaphylaxis
atopic dermatitis
venom
109
Q

symptoms of type 1 hypersens

A 
hives
difficulty breathing
swelling
hypotension
anaphylaxis
110
Q

describe type 2 hypersens

A

Ab that is directed against cell surface markers or the ECM

  • complement and Fc receptor-induced recruitment and activation of leukocytes (bring in neutrophils and macrophages eliciting tissue damage)
  • opsonization and phagocytosis
  • cell function abnormalities by competitive inhibition or activation
111
Q

discuss the mechanisms of complement and Fc receptor mediated type 2 hypersens

A

Abs bind to activate the neutrophil
complement activation releases C3a and C5a to activate the neutrophil
neutrophils generate ROS and lysosomal enzymes that cause inflammation/injury
can occur after strep infection due to antibody cross reacting with myocardium and myocarditis

112
Q

discuss the mechanisms of opsonization and phagocytosis mediated type 2 hypersens

A

complement activation occurs releasing C3b that opsonizes the cell
Fc receptor on phagocytes recognizes C3b on an opsonized cell and phagocytoses the infected cell

113
Q

type 2 hypersens against blood products

A

may occur with erythrocytes and platelets causing anemia and thrombocytopenia

114
Q

discuss cell function abnormalities by competitive inhibition or activation that occur w type 2 hypersen

A

Abs generated against hormone receptors competitively inhibit hormone production

  • graves
  • myasthenia gravis
115
Q

graves

A

thyroid stimulation even in the absence of TSH leading to hyperthyroidism

116
Q

myasthenia gravis

A

MSK paralysis disease where Abs are made against the Ach receptor and inhibit transmission of signals to muscle to move

117
Q

type 3 hypersens

A

disease is caused by deposition of circulating Ab/Ag complexes in blood vessels

  • activation of complement
  • activation of inflammatory cascade
118
Q

symptoms of type 3 hypersens

A

systemic or localized
vasculitis
nephritis
inflammatory skin reaction

119
Q

arthus rxn

A

localized Ag/Ab complex deposition

due to vaccine, local vasculitis

120
Q

example of arthus rxn

A

tetanus vaccine

  1. pt gets the tetanus vaccine
  2. development of normal Abs to tetanus toxoid
  3. repeat vaccination occurs within a short time
  4. pre-formed antibodies complex with additional vaccine antigen and deposit in the subQ tissue
  5. localized inflammation, pain, swelling
121
Q

examples of type 3 hypersens diseases

A 
SLE
polyarteritis nodosa
post-strep glomerulonephritis
serum sickness
arthus rxn
122
Q

type 4 hypersens

A

T lymphocyte mediated delayed hypersens

T cells can cause disease by causing tissue injury

123
Q

4 types of type 4 hypersens

A
  1. local autoimmune reaction with T cells directed against cellular antigens within that local tissue
  2. persistent response to environmental triggers
  3. T cell response to microbes
  4. response to superantigens
124
Q

classic type 4 hypersens microbe

A

tuberculosis- granulomatous inflammation because of persistent infection causing local tissue injury

125
Q

superantigens

A

bacterial and viral toxins that bind to T cell receptors regardless of specificity causing inflammation trough excessive cytokine production

126
Q

mechanism of type 4 hypersens

A

same as for attacking microbes, but antigen may never be cleared
CD4+ cells targeting cell or tissue Ags presented by APCs
CD8+ cells targeting host cells
may work together

127
Q

type 4 hypersens diseases

A 
multiple sclerosis
rheumatoid arthritis
DM1
IBD (crohns)
contact sensitivity (poison ivy, metal allergy)
chronic infection (tuberculosis)
viral hepatitis (hep B and C)
toxic shock
128
Q

how do DTH skin tests work

A

must have prior exposure to develop sensitivity
T cells home to the site
-respond to the antigen
-T cells and monocyte infiltration
-CD4+ cytokine production causes increased vascular permeability, leading to edema and fibrin deposition
-leukocyte products lead to tissue damage

129
Q

type 2 hypersens diseases

A 
autoimmune hemolytic anemia
autoimmune thrombocytopenic purpura
goodpastures
graves disease
myasthenia gravis
pemphigus vulgaris
pernicious anemia
rheumatic fever

MM Test 2 (23 decks)

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