MM Test 2 > B6.026 Autoimmunity > Flashcards

B6.026 Autoimmunity Flashcards

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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
PRRs
pattern recognition receptors innate immune receptors that recognize PAMPs and DAMPs toll-like receptors nod-like receptors
26
toll like receptors (TLRs)
specific for microbial components | activate transcription factors to stimulate expression of genes encoding cytokines, enzyme, and other proteins
27
TLR signaling process
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
28
nod like receptors (NLRs)
family of cytosolic receptors that sense DAMPs and PAMPs in the cytoplasm
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NOD-1 and NOD-2
contain N-terminal CARD (caspase related domains) bacterial peptidoglycans in the cell wall activates NF-kB
30
NLRP-3
recognizes microbial products, substances associated with cell damage, and endogenous substances in cells in large quantities (crystals) enhances production of IL-1B
31
describe the inflammasome
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
32
inflammasome dysregulation associated conditions
gout- urate crystal deposit | auto inflammatory syndromes (familial periodic fear syndromes)
33
process of leukocyte recruitment
1. rolling 2. integrin activation by chemokines 3. stable adhesion 4. migration through endothelium (diapedesis)
34
characterize neutrophils
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
35
function of neutrophils
phagocytose microbes in the blood and in tissues and destroy them through the oxidative burst recruited to tissues to remove debris
36
lifespan of neutrophils
live for only a few hours | dead ones form pus
37
characterize monocytes/macrophages
found in all connective tissue and organs | prolonged survival in tissues
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function of macrophages
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
39
classical macrophage activation
``` immune signals -TLRs -cytokine INFy from innate and adaptive immunity produces M1 activated macrophages destroy microbes and induce inflammation ```
40
alternative macrophage activation
cytokines IL-4 and IL-13 (same as associated w allergies) produces M2 activated macrophages tissue repair and termination of inflammation (downregulate immune system)
41
dendritic cells
APCs initiation production of cytokines, and thus initiate inflammation bridge innate and adaptive immunity -stimulate adaptive immune responses
42
characterize mast cells
abundant cytoplasmic and vasoactive granules | located on skin and mucosal epithelium
43
how are mast cells activated
microbial products binding to TLRs (innate) | antibody dependent- typically IgE mediated type 1 hypersensitivity reactions
44
function of mast cells
vasoactive amines (histamine and tryptase) -increased capillary permeability -kill bacteria and inactivate microbial toxins synthesize and secrete lipid mediators and cytokines -stimulate inflammation
45
NK cell markers
CD16+/56+
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primary function of NK cells
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
47
other uses of NK cells
fight intracellular microbial infections | secrete IFN-y for macrophage activation
48
how are NK cells activated
by macrophages and dendritic cells IL-15: development and maturation of NK cells IL-12 and IFN type 1: enhance NK cell killing function
49
inhibition of NK cells
block signaling by receptor activation specific for self MHC 1 molecules to protect healthy cells via ITIMs
50
function of ITAMs
eliminate cells infected with intracellular microbes via antibody dependent cellular cytotoxicity (ADCC)
51
alternative complement pathway
triggered when activated complement proteins on microbial surfaces are uncontrolled due to lack of regulatory proteins innate immunity
52
classical complement pathway
triggered by antibodies bound to microbes/antigens | adaptive immunity
53
lectin pathway
mannose binding lectin binds to terminal mannose residues | innate immunity
54
function of activated complement proteins
1. opsonization and phagocytosis (C3b) 2. inflammation (C5a, C3a) 3. MAC cell lysis
55
plasma proteins of innate immunity
increase rapidly with infection = acute phase response - collectins - CRP
56
collectins
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
CRP
binds phosphorylcholine on microbes, opsonizes them for phagocytosis by macrophages activates classic complement pathway proteins non specific marker of inflammation
58
what are interleukins
soluble proteins that cause cell signaling to generate immune and inflammatory reactions - stimulated by infection communication between cells
59
cytokines that stimulate APR protein synthesis from the liver (CPR and fibrinogen)
IL-6
60
cytokines for recruitment of neutrophils and monocytes
TNF IL-1 chemokines
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cytokines that cause fever by acting on the hypothalamus
TNF | IL-1
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source of TNF
macrophages T cells mast cells
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effects of TNF
``` endothelial cell activation neutrophil activation fever synthesis of APR in liver catabolism of fat and muscle apoptosis ```
64
source of IL-1
``` macrophages dendritic cells endothelial cells some epithelial cells mast cells ```
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effects of IL-1
endothelial cell activation fever synthesis of APR in liver TH17 differentiation
66
source of chemokines
``` macrophages dendritic cells endothelial cells T lymphocytes fibroblasts platelets ```
67
effects of chemokines
leukocytes: increased integrin affinity, chemotaxis, and activation
68
source of IL-12
dendritic cells | macrophages
69
effects if IL-12
INFy production and increased cytotoxic activity of T cells and NK cells Th1 differentiation
70
source of IFN-y
NK cells | T lymphocytes
71
effects of IFN-y
activation of macrophages | stimulation of some Ab response
72
source of type 1 IFNs (a and B)
IFNa: dendritic cells, macrophages IFNB: fibroblasts
73
effects of type 1 IFNs
antiviral state increased MHC 1 expression NK cell activation
74
source of IL-10
macrophages dendritic cells T cells
75
effects of IL-10
acts on dendritic cells and macrophages inhibition of cytokine and chemokine production reduced expression of co-stimulators and MHC 2 molecules
76
source of IL-6
macrophages endothelial cells T cells
77
effects of IL-6
synthesis of acute phase proteins in liver | proliferation of Ab producing B cells
78
source of IL-15
macrophages
79
effects of IL-15
proliferation of NK and T cells
80
source of IL-18
macrophages
81
effects of IL-18
IFNy synthesis in NK and T cells
82
source of TGF-B
many cell types
83
effects of TGF-B
inhibition of inflammation | differentiation of Th17 and Treg cells
84
how do innate immune cells discriminate against self antigens
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
how do adaptive immune cells discriminate against self antigen
lymphocytes that recognize self undergo apoptosis or are inactivated when they encounter self antigen
86
primary function of B lymphocytes
neutralization of microbe, phagocytosis, and complement activation VIA production of antibodies (IgD,A,M,G,E)
87
membrane bound antibodies
function as B cell receptor
88
which Ig is secreted onto mucosa
IgA
89
which Igs are present on naïve B cells
IgM and IgD | not as important for response to antigens
90
most abundant Ab in plasma
IgG
91
which Ig crosses the placenta
IgG
92
plasma cells
long living mature B cells | produce high affinity antibodies even after antigen removal in response to vaccines and infections
93
memory B cells
long living mature B cells do not produce Ab rapidly respond with antigen re-exposure
94
T cell dependent B cell response
``` 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
T cell independent B cell response
polysaccharides, lipids, and other non protein antigens elicit Ab production without involvement of T cells low affinity, short lived
96
primary antibody response
within days IgM produced/wanes low affinity plasma cells go on to produce IgG long term
97
secondary antibody response
within days larger response IgG higher affinity
98
describe B cell receptor signaling via complement receptors
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
describe B cell receptor signaling via TLRs
promote B cell proliferation, differentiation, and antibody secretion
100
intracellular portion of BCR signaling
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
positive selection
selects for cells that express a BCR
102
negative selection
selects against cells with a BCR that binds self antigen with high affinity -undergoes BCR editing or clonal deletion if self reactive
103
hypersensitivity type and test mnemonic
1. A 2. C 3. I 4. D
104
what is the general definition of hypersensitivity
injurious or pathologic immune reactions | exaggerated and abnormal reactions
105
2 mechanisms of hypersensitivity
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
4 types of hypersensitivity
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
describe type 1 hypersensitivity
true allergy or atopy | IgE antibody-mast cell mediated in response to an antigen
108
examples of type 1 hypersens
``` allergic rhinitis/conjunctivitis food/med allergies asthma anaphylaxis atopic dermatitis venom ```
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symptoms of type 1 hypersens
``` hives difficulty breathing swelling hypotension anaphylaxis ```
110
describe type 2 hypersens
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
discuss the mechanisms of complement and Fc receptor mediated type 2 hypersens
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
discuss the mechanisms of opsonization and phagocytosis mediated type 2 hypersens
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
type 2 hypersens against blood products
may occur with erythrocytes and platelets causing anemia and thrombocytopenia
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discuss cell function abnormalities by competitive inhibition or activation that occur w type 2 hypersen
Abs generated against hormone receptors competitively inhibit hormone production - graves - myasthenia gravis
115
graves
thyroid stimulation even in the absence of TSH leading to hyperthyroidism
116
myasthenia gravis
MSK paralysis disease where Abs are made against the Ach receptor and inhibit transmission of signals to muscle to move
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type 3 hypersens
disease is caused by deposition of circulating Ab/Ag complexes in blood vessels - activation of complement - activation of inflammatory cascade
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symptoms of type 3 hypersens
systemic or localized vasculitis nephritis inflammatory skin reaction
119
arthus rxn
localized Ag/Ab complex deposition | due to vaccine, local vasculitis
120
example of arthus rxn
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
examples of type 3 hypersens diseases
``` SLE polyarteritis nodosa post-strep glomerulonephritis serum sickness arthus rxn ```
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type 4 hypersens
T lymphocyte mediated delayed hypersens | T cells can cause disease by causing tissue injury
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4 types of type 4 hypersens
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
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classic type 4 hypersens microbe
tuberculosis- granulomatous inflammation because of persistent infection causing local tissue injury
125
superantigens
bacterial and viral toxins that bind to T cell receptors regardless of specificity causing inflammation trough excessive cytokine production
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mechanism of type 4 hypersens
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
type 4 hypersens diseases
``` 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
how do DTH skin tests work
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
type 2 hypersens diseases
``` autoimmune hemolytic anemia autoimmune thrombocytopenic purpura goodpastures graves disease myasthenia gravis pemphigus vulgaris pernicious anemia rheumatic fever ```
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