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Host and Defense > Week 12 > Flashcards

Week 12 Flashcards

1
Q

What is the purpose of acute inflammation?

A

Eliminate the initial cause of cell injury

Clear out necrotic cells and tissue damaged from original insult and inflammatory process

Initiate tissue repair

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2
Q

Too little inflammation can lead to…

Too much inflammation can lead to….

A

Progressive tissue destruction and compromise the survival of the organism

A host of diseases such as cardiovascular disease, cancer, Alzheimer’s, neurological diseases, arthritis, autoimmune diseases, diabetes 2, pulmonary diseases

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3
Q

What is the goal of antiinflammatory therapy?

A

Decrease inflammation

Decrease pain

Arrest tissue destruction

Preserve function

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4
Q

True or false.. chronic inflammation involves an ongoing stimulus, lasts weeks, and is absent in any cardinal signs, and the fundamental cells ar lymphocytes, macrophages, and fibroblasts (whereas acute is neutrophils and macrophages)

A

True

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5
Q

NSAIDs inhibit ____

A

Cyclooxygenase enzymes (COX enzymes)

This decreases pain and inflammation through inhibiton of prostaglandin synthesis.

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6
Q

Glucocorticoids inhibit ____

A

Phospholipase A2

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7
Q

What are DMARDs? What are the two types?

A

Disease modifying anti-rheumatic drugs

Traditional (non-biologic) DMARDs

Biologic DMARDs

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8
Q

What are eicosanoids?

A

Oxygenation products of poly-unsaturated long-chain fatty acids

Act in autocrine/paracrine fashions

Includes prostanoids

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9
Q

What are prostanoids?

A

Subclassification of eicosanoids including…

Prostaglandins -mediators of inflammatory response

Thromboxanes - mediators of vasoconstriction

Prostacyclin - active in the resolution of inflammation

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10
Q

Prostanoids have major biological effects on what 5 things?

A

Smooth muscle

Platelets and blood cells

Nerve terminals

Endocrine organs

Adipose tissue

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11
Q

COX2 selective inhibitors have reduced ___ adverse effects but ma increase risk of thrombosis, stroke, or kidney failure.

These drugs do not inhibit ___ or cause ____

A

GI

Platelet aggregation

GI upset/ulceration

(Note that this means that COX1 is responsible for GI upset, so COX2 selective inhibitors do not have these effects)

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12
Q

The NSAID Aspirin (AKA acetylsalicylic acid) inhibits _____. It is the only NSAID to inhibit both COXs in an ____ manner. This drug is valued primarily for its _____ effects when used regularly.

A

COX1 and COX nonselectively

Irreversible

Anti-platelet aggregation

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13
Q

True or false… aspirin is regularly used as an anti-inflammatory medication

A

False… it is mostly just used for its antitrhrombotic effects

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14
Q

What are aspirin’s contraindications?

A

Avoid in children with viral-induced illness (reye syndrome)

Avoid in patients with NSAID allergies, renal insufficiency, gout, bleeding disorders,

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15
Q

Ibuprofen is an NSAID derived from ____. Ibuprofen should not be taken with ____ because ibuprofen interferes with the ____ effect of low-dose ____, making it less effective for MI and stroke prevention.

A

Propionic acid

Aspirin

Antiplatelet

Aspirin

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16
Q

What is naproxen?

A

Similar in pharmacological profile as other NSAIDs but available in slow-release formulation

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17
Q

Name some adverse effects common to all NSAIDS

A

GI issues: abdominal pain, dysplasia, nausea, vomiting, ulcers

Reye syndrome: in children taking salicylates after viral induced illness. Potentially fatal

CNS
Skin
Renal
Hematological

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18
Q

Name three NSAIDs

A

Aspirin

Ibuprofen

Naproxen

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19
Q

What is celecoxib? What is it used to treat?

A

It is a cox-2 selective inhibitor (it is 10-20x more selective for cox-2 than cox-1)

Used to treat osteoarthritis, rheumatoid arthritis, ankylosing, and painful menstration

No effect on platelet aggregation

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20
Q

What is acetaminophen? What is its mechanism?

A

It is a non-aspirin pain reliever (tylenol)

Relieves fever, headaches , mild pains.

Not anti-inflmmatory (not an NSAID)!!!

Mechanism - centrally acting effect on hypothalamus to cause vasodilation and sweating (reduces fever), also elevates the pain threshold.

Overdose can result in hepatotoxicity

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21
Q

What are glucocorticoids? What is its mechanism? Their anti-inflammatory effect results from…

A

Steroid hormones

Prevents conversion of membrane phospholipids to arachidonic acid by inhibiting the phospholipase A2 enzyme (which is a critical step in the formation of inflammatory mediators)

Inhibiton of phospholipase
Alteration in lymphocytes
Inhibition of cytokine expression
Stabilization of the cellular membrane

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22
Q

What are some adverse effects of glucocorticoids?

A 
Cardiovascular risk
Cataracts 
Skin thinning 
Gastric ulcer 
CNS problems
Osteonecrosis/porosis
Myopathy 
Infections
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23
Q

Name three short to medium acting glucocorticoids

A

Hydrocortisone

Cortisone

Prednisone

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24
Q

Name one long-acting glucocorticoid.

A

Dexamethasone

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25
Q

Prednisone is an immunosuppressant drug once converted to its active metabolite ___ via ___ metabolism. Describe its mechanism of action

A

Prednisolone

Hepatic metabolism

Blocks phospholipase A2, thus shuts down immune responses

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26
Q

True or false… DMARDs can actually suppress the progression of the disease through their actions against the underlying immunological abnormalities.

A

True

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27
Q

What DMARD is the first line for rheumatoid arthritis?

A

Methotrexate

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28
Q

What is the mechanism of methotrexate?

A

Inhibits transformylase and thymidylate synthetase enzymes (leading to the inhibiton of pro-inflammatory cytokines and inhibiton and apoptosis of immune inflammatory cells)

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29
Q

Name two DMARDs

A

Methotrexate

Azathioprine

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30
Q

True or false… methotrexate may be taken in pregnancy

A

False. It is contraindicated in pregnancy

Also… there is a risk of serious life-threatening adverse effects if taken with NSAIDs

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31
Q

What is the mechanism, clinical use, and adverse effects of azathioprine?

A

Mechanism - prodrug that acts through its main metabolite 6-thioguanine to strongly suppress DNA synthesis in and production of rapidly proliferating immune cells

Clinical uses - approved for RA and kidney transplant rejection prophylaxis

Adverse effects - bone marrow suprression, GI upset

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32
Q

What are biologic DMARDs? Give some examples

A

Proteins produced by recombinant DNA technology

T-cell modulators and TNF-alpha blocking agents, and others

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33
Q

What is the mechanism, clinical use, and adverse effects of abatacept?

A

Mechanism - acts as a fusion protein to prevent activation of T cells

Clinical use - treatment of RA in patients whom have failed to respond to anti TNF-alpha therapy

Adverse effects - increased risk of lymphomas, infections, congestive heart failure

Very expensive drug!

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34
Q

True or false… there are 5 different TNF-alpha inhibition biologic dMARDs clinically available

A

True

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35
Q

What is the mechanism, clinical use, and adverse effects of adalimumab?

A

Mechanism - Prevents ligand from binding to TNF-alpha receptor.

Clinical uses - rheumatoid arthritis, ankylosing spondylitis, inflammatory bowel disease

Adverse effects - increased risk of lymphomas, infections, congestive heart failure

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36
Q

True or false… plasma cells have the potential to differentiate into memory B cells

A

False

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37
Q

The chemokines ___ attracts immature B cells to HEV, then ___ and ___ attract the B cell into the lymph node. Then the chemokines __ attracts the B cells into the primary follicle of the lymph node

A

CCL21

CCL21 and CCL19

CXCL13

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38
Q

In the primary follicle, ___ is released form the B cell which binds to a receptor on a _____. Then, this cell releases ____to activate the B cell

A

Lymphotoxin

FDC (follicular dendritic cell)

BAFF (B cell activating factor)

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39
Q

What are follicular dendritic cells?

A

They are not really dendritic cells. They are more like stromal cells involved in B cell development

Accumulate antigens via complement receptors

No phagocytosis activity

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40
Q

Where are B cells presented antigen?

A

Lymph nodes

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41
Q

B cell activation drives…

A

Clonal expansion

Class switching

Somatic hypermutation

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42
Q

In the lymph node, antigen is presented to B cells from FDCs and subcapsular sinus macrophages by ___

A

Cr2

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43
Q

What is the role of Cd3 in the activation of B cells?

A

Cd3 targets the antigens so the macrophages and follicular dendritic cells can hold onto it.

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44
Q

What are the two different types of antigen that can activate a B cell?

A

Thymus-dependent antigen

Thymus independent antigen

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45
Q

What antigen type is typically protein? What type is non-protein? What type of antigen presentation is most common?

A

Thymus-dependent antigen is typically protein

Thymus-independent is typically non-protein antigen.

Thymus-dependent is most common

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46
Q

What three signals are involved in thymus-dependent antigen?

A

Antibody crosslinking - activation

Co-receptor signals - survival and proliferation

Cytokines - differentiation, class switching, somatic hypermutation

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47
Q

What signals are involved in thymus-independent antigen presentation?

A

PRR-detected antigen

Complement bound to co-receptor

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48
Q

True or false… in thymus-dependent antigen presentation, a TFH cell (T follicular helper cell) is required

A

True

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49
Q

Describe the process of antibody crosslinking signaling

A

B-cell receptors bind antigen, resulting in clustering of the receptors.

Clustering of antigen receptors allows receptor-associated kinases to phosphorylate the ITAMs leading to activating signals. (Igalpha and Igbeta signaling)

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50
Q

What is the purpose of the co-receptor signals in the activation of B cells?

A

Ensures the target is pathogenic (as opposed to self)

Prevents the B cell from becoming anergic

Initiates clonal expansion

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51
Q

What are some things that coreceptors in B cells can bind?

A

Complement

PRRs (bind many different things)

CD40 receptors

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52
Q

What co-receptor complex binds C3d (complement)

A

CR2 bound to CD19 and CD81

This receptor complex must be activated in close timing and proximity to the antibody receptors in order to induce synergistic activation signals

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53
Q

____ cells are the most common source of cytokines during B cell activation. ____ cytokines can provide signals in the absence of T cell-mediated activation .

A

TFH

Local

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54
Q

What are the four roles of cytokine signaling in B cell activation?

A

Survival and proliferation

Class switching (same epitope binding, different heavy chain)

Somatic hypermutation (increases antibody specificity)

Differentiation (produces plasma cells and memory B cells)

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55
Q

B and t cells come together to form ____ at the follicle boundary. Describe how these form.

A

Cognate pairs

Naive B cells search for specific antigen displayed by FDCs in the B cell area. Meanwhile, naive T cells search for specific antigen displayed by dendritic cells in the T cell area.

Antigen activated T cells proliferate/differentiate. Antigen-activated B cells move to the boundary region

Antigen-activated B cells present antigen to effector TFH cells, forming cognate pairs.

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56
Q

True or false… if a B cell has an receptor for a lipid antigen, it will not form a cognate pair

A

True, because it will undergo thymus-independent antigen activation

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57
Q

True or false… TFH cells drive B cell activation, proliferation, enhanced specificity, and differentiation into plasma and memory cells

A

True

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58
Q

True or false.. thymus independent activation typically yields a larger population of plasma and memory cells

A

False… Thymus dependent activation (TFH) activation typically does

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59
Q

Describe how TFH cells aid in B cell activation

A

B cell is first activated by antigen binding

B cell the presents antigen to TFH cells

CD40 is a receptor on B cells that is stimulated by a CD40 ligand on T cell. This will induce survival and proliferation of B cells

Cytokines: differentiate and/or isotype switch

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60
Q

B cells form plasma cells in two stages and places. What are they?

A

Cognate pairs first move to the primary focus (medullary cords)

Cognate pairs then move to the secondary focus (located in the primary follicle) and form germinal centers

Note that the cognate pairs must cross the T-cell area in order to get from medullary cords to primary follicle

61
Q

What occurs in the primary focus (medullary cords) in regards to the formation of plasma cells?

A

Production of IgM expressing plasma cells for several days

No class-switching or somatic hypermutation

62
Q

Where is the boundary region in lymph nodes?

A

Located between the primary follicle and T cell area. This is where cognate pairs are first formed

63
Q

Describe what occur in the secondary focus in regards to the production of plasma cells

A

Cognate pair moves to the secondary focus in which a germinal center is formed and the following occurs…

Enormous proliferation and plasma/memory cell production

Class switching and somatic hypermutation

Selection of most specific plasma cells

64
Q

B cells hypermutate and class switch in ____

A

Germinal centers

65
Q

Cognate pairs form germinal centers in the ___ zone. What cells are found here?

A

Follicular

TFH cells

Follicular dendritic cells

Centroblasts

Centrocytes

66
Q

What are centroblasts?

A

Form the germinal center dark zone

Proliferating source of new B cells

Do not express surface immunoglobulin

Somatic hypermutation occurs

Class switching occurs

Centroblasts form centrocytes

67
Q

True or false.. centroblasts directly form plasma and memory cells

A

False… centrocytes form plasma cells and memory cells

68
Q

What are centrocytes?

A

Form the light zone

Divide slowly

Express surface immunoglobulin

Cannot class switch or hypermutate

Interact with and selected by FDCs

Programmed to die

69
Q

True or false… class switching and somatic hypermutation improve antibody specificity

A

True

70
Q

In order for class switching to occur, ___ proteins are reactivated which will cause a change in the ____ ___ region of the antibodies produced. Class switching is ___ induced.

A

RAG

Heavy chain Fc

Cytokine

71
Q

True or false… different cytokines yield different isotypes to be produced.

A

True

72
Q

True or false… different classes of antibodies dictate effector functions

A

True

73
Q

What is somatic hypermutation?

A

Directed hypervariable region mutations by single nucleotide insertions and substitutions yielding new epitope binding regions increasing antibody affinity.

Somatic hypermutation is paired with selection processes.

74
Q

True or false.. as centroblasts divide, less mutations (somatic hypermutation) are produced

A

False… more mutations are produced

75
Q

True or false… since centrocytes have undergone the first round of somatic hypermutation, they produce a new antibody that is different than the cognate B cell antibody

A

True

76
Q

Only centrocytes that bind FDCs can bind to ___

A

TFH cells

77
Q

What happens when FDC-bound centrocytes are bound by TFH cells? (5 things)

A

Limited TFH cell population in the germinal center

Survival signal

Selection of centrocytes with the highest antibody affinity

Further proliferation

Differentiation into plasma cells or memory B cells

78
Q

Name some differences between naive B cells and plasma cells

A

Naive B cells produce surface Ig, have a surface MHC class 2, can undergo isotype switching, can grow, can undergo somatic hyper mutation

Plasma cells have a high ig secretion

79
Q

True or false… all plasma cells will be found within the lymph nodes

A

False… some go to the site of infection

80
Q

Antibodies have four broad effector functions. What are they?

A

Virus/toxin neutralization

Opsonization

Complement fixation/activation

Antibody-dependent cell-mediated immunity (targeting self infected cells)

81
Q

What antibodies will you find in internal tissues?

A

IgM
IgA
IgG

82
Q

What antibodies are found at mucosal surfaces?

A

IgA

83
Q

What antibody is used for parasite immunity?

A

IgE

84
Q

What antibody is a B cell receptor?

A

IgD

85
Q

Fc receptors can be monomeric or dimeric, but often involve ____ for activation

A

Dimerization

86
Q

There are Fc receptors for what classes of antibodies?

A

IgE
IgA
IgG

87
Q

Fc receptors can have stimulatory or inhibitory signaling when bound to an antibody. What things may happen?

A

Phagocytosis
Degranulation
Targeted killing
Cytokine production/release

88
Q

Name two functions of Fc receptors

A

To enhance innate immunity by stimulating or inhibiting signals

Involved in Ig transport

89
Q

Explain how Fc receptors facilitate IgG transport into tissues

A

Cytokines upregulate Fc receptors on the endothelial cells of blood vessels. The receptors bind antibody and bring in the antibody (acidic pH in the vesicle causes an interaction with Fc receptor to protect the antibody from proteolytic). Then the antibody is released into the inflamed tissue by exocytosis

90
Q

Explain how transcytosis of IgA protects mucosal surfaces.

A

IgA binds to an pIgR ((poly-Ig receptor) IgA Fc receptor) on basolateral side of epithelial cell. Receptor mediated endocytosis of antibody occurs and transports the IgA to apical side of cell. Receptor is cleaved, but IgA remains bound to mucus through the secretory piece

91
Q

Which classes of antibodies are capable of neutralizing antibodies to prevent pathogen establishment? Explain how it works

A

IgA and IgG

Antibody binding to viruses will prevent the viruses ability to infect/penetrate cells

Antibody binding to strep. Pyogenes will prevent bacteria from attaching to surfaces

92
Q

Explain how erythrocytes clear agglutinized antigens

A

Antibody complexes form within blood which bind antigen. Complement binds to antibody complex. Erythrocytes binds to complement -antigen-antibody complex. This erythrocytes carries this complex to liver or spleen where macrophages take up the immune complex

93
Q

Explain how IgE makes mast cells, basophils, and eosinophils competent

A

IgE binds to these cells to become these cells’ receptors. Mast cells, for example remained in a fixed location and accumulate many different types of of IgE. Then when one of these receptors are stimulated, they degranulate. This is important in allergic responses

94
Q

True or false… IgM and IgG initiate the complement cascade.

A

True. IgM is typically better at initiation

95
Q

Describe how antibody-dependent cellular cytotoxicity works

A

Anti CD20 antibody binds to CD20 on the surface of abnormal self cells (cancer) Fc receptors on NK cells recognize anti-CD20 antibody and degranulate

96
Q

Antibodies provide passive immunity during development. … ____ during gestation. ____ protects infant mucosal surfaces (from breast feeding) In these ways, the mothers immunity is passed on to the child

A

IgG

IgA

97
Q

What are two roles of NK cells?

A

Destroy diseased and dysfunctional self-cells

Interface between adaptive and innate immune system

98
Q

NK cells are developmentally similar to ___ cells

A

T cells

99
Q

True or false… NK cells may form memory cells

A

True

100
Q

Positive and negative signal balance determines NK cell killing. Describe the three cell states that regulate NK cell targeting.

A

Protection - healthy cells express low amounts of stimulatory ligand but also MHC-1 which. Inhibitory signal from MHC-1 overrides stress signal

Missing self - unhealthy cells reduce MHC-1 expression so that the stimulatory signal of the stress ligands override the inhibitory signal. This will result in NK cells killing the target cell

Induced self - unhealthy cells increase stress ligand expression. This causes the stimulatory signal to override the inhibitory signal, leading to death of the target cell

101
Q

True or false.. all NK cells detect all MHC1 receptors or stress ligands

A

False

102
Q

NK cells have activating and inhibitory receptors. Name two activating receptors and two inhibitory receptors

A

Activating:
NKG2D (preferentially binds MIC)
CD16 (Fc receptor) (this binds to MIC proteins)

Inhibitory:
NKG2A (preferentially binds MHC)
KIR family

103
Q

True or false… all NK cells in the body have the same combinations of receptors

A

False.. NK cells express diverse combinations of receptors

104
Q

What are the three major receptor families for NK cells?

A

CD16: low affinity IgG Fc receptor; activating receptor

NKG family

KIR family (Killer-cell immunoglobulin-like receptors) - bind MHC1, inhibits NK cell activation, detects healthy self tissue

105
Q

True or false… NK cells usually express NKG2A and KIR receptors at the same time

A

False. Typically one or the other

106
Q

What is the significance of having multiple isotypes of MHC1?

A

Each isotype has variance, which allows the MHC1s to bind to lots of different antigen.

107
Q

Describe NK cell education

A

MHC1 exposure during development

NK cells detect that specific MHC1 isotype

NK cells must detect that MHC1

NK cells only detect that MHC1

108
Q

HLA-E is recognized by….

A

CD94:NKG2A

109
Q

What detects the following…
HLA-A, B, C

HLA-E, G

HLA-F

A

HLA-A, B, C - T cell and NK cell receptors

HLA-E, G - NK cell receptors

HLA-F, - Intracellular chaperone

110
Q

What three things activate NK cells?

A

Target cell interaction (down regulated MHC1, Stress ligands, CD16)

Leukocyte interaction (antigen presenting cells, Th cells, NKT cells)

Cytokines (IFNs, IL-12, proliferation , receptor expression, cytokines, granule production)

111
Q

What are the effector functions of NK cells?

A

Cytokine release

Cytotoxicity

112
Q

Explain NK activation via innate immune system

A

Multiple (2) signals are required

MHC surveillance

Stress ligands

113
Q

Explain how the adaptive immune system may activate NK cells

A

On signal from antibodies are required. Fc binds to CD16 on NK cells to activate them

This signal is an override signal than will result in death of the target cells (covered in antibodies)

114
Q

Describe Nk cell cytotoxicity (3 things)

A

Degranulation (perforins and granzymes)

Death-receptors (FasL, TRAIL)

Interferons and NO

115
Q

What is the major role of gamma-delta T cells? Where are they prominently found?

A

Major role: remove diseased and malignant cells

Prominent in tissues and mucosal surfaces (as opposed to blood) - sit in epithelial layers. Intraepitheilal lymphocytes

116
Q

What kind of antigens do gamma-delta T cells bind?

A

Lipids

Phospholipids

Phosphoantigens (phosphorylated proteins)

117
Q

What are the effector functions of gamma delta T cells?

A

They have both CD8 and CD4 -like activity. Direct killing. Cytokine and chemokine release. NK, macrophage, and DC activation

Can be APCs and migrate to lymph nodes

Similar to NK cells in that they express stress-ligand receptors and they also detect the presence of MHC

Promote tissue repair

118
Q

What is the role of CD1?

A

Expresses self and non-self lipids. Interacts with gamma delta T cells to discriminate self vs. nonself. Will drive activation, and potential targeting killing. Co signal dependent

119
Q

True or false… because CD1-gamma delta T cell interactions are highly specific, they are co-signal dependent

A

True

120
Q

What three things do gamma delta T cell receptors bind?

A

Phospholipid receptors

MHC1-related receptors

Stress ligands

121
Q

Gamma delta T cells drive inflammation by…

A

Th17 and Th1 and NK cell activation (locally)

122
Q

Gamma delta T cells are directly cytotoxic by releasing…

A

Perforin and granzyme

CD16

123
Q

How do delta gamma T cells drive the adaptive immune system?

A

They stimulate DC and macrophages

They are APCs

124
Q

Delta gamma T cells have relatively rapid responses to local pathogens and disease. They react to …

A

PAMPs

Stress ligands

125
Q

Mucosal surfaces are widespread and prominent sites of infection. What is the number one world wide cause of death from mucosal surface infections?

A

Acute respiratory infections

126
Q

What are the three tracts within the body that have mucosal surfaces?

A

Respiratory tract

Gastrointestinal tract

Urogenital tract

127
Q

Intestinal lymphocytes are found in ___ tissues where immune responses are induced and ____ ____ the intestine, where they carry out effector functions

A

Organized

Scattered throughout

128
Q

What are the three compartments of mucosal tissues?

A

Epithelium

Lamina propria

Mucosal associated lymphoid tissue (MALT)

129
Q

True or false… the epithelium in the mouth and the gut are both single layered

A

False. The gut epithelium is single layered whereas the mouth is multilayered

130
Q

What are the immune cells found within the epithelium of mucosal tissues?

A

Intraepithelial lymphocytes.. which include the following…

Delta gamma T cells
CD8 a:a T cells
Memory CD8 cells

131
Q

What immune cells are found within the lamina propria of mucosal tissues?

A

Delta gamma T cells

CD8 T cells

CD4 T cells (Th1, Th17)

Plasma cells and memory b cells

Macrophages

Dendritic cells

132
Q

In the oral mucosal system.. the tonsils and adenoids form a ring of lymphoid tissues called ____, around the entrance of the gut and airway

A

Waldeyer’s ring

133
Q

True or false… mucosal infections follow the traditional inflammatory pathway

A

False

134
Q

Mucosal immunity often employs limited ____. In fact, most infections are often cleared ___ an inflammatory response. It has a ____ proactive and ____ reactive immunity. Both ____ and ___ cells respond. Neutrophils are only recruited if the infection is _____

A

Inflammation

Without

Strong

Limited

Local innate

Adaptive cells

Severe, persistent, and/or causes tissue damage

135
Q

Mucosal surfaces have unique immune features. Name the unique anatomical, features, effector mechanisms, and immunoregulaory environment

A

Anatomical: intimate interactions between mucosal epithelia and lymphoid tissues. Specialized antigen uptake mechanisms (M cells)

Effector mechanisms: secretory IgA. Activated/memory T cells predominate even in absence of infection.

Immunoregulatory enviornment: active downregulation of immune responses. Inhibitory macrophages and tolerance-inducing dendritic cells

136
Q

Naive lymphocytes are activated in ____ to give rise to effector cells that will travel in the lymph and blood to gain access to the ____ of the mucosal tissue, or become ___

A

Peyer’s patches

Lamina propria

Interepithelial lymphocytes

137
Q

As you progress down the GI tract, you get more and more of what genus of bacteira?

A

Bacteroidetes

138
Q

True or false… The oral microbiome is diverse and changes with disease. Diversity and richness increases with disease

A

True

139
Q

How is the microbiome constantly shaped at mucosal surfaces?

A

Antigens are taken up in peyer’s patches in lymphoid follicles

Local immune responses activate protective mechanisms that stabilize the epithelial barrier (release antimicrobial peptides and IgA)

CD4 Th17 are important

140
Q

The mucosal microbiome affects the local cytokine environment and subsequently CD4 T cell differentiation. Describe this relationship.

A

TGF-beta with inflammatory cytokines will lead to Th17 cells (these cells drive inflammation by neutrophil recruitment, antimicrobial peptide production, and tissue repair)

TGF-beta without inflammatory cytokines will lead to TReg cells (these cells inhibit mucosal inflammation)

141
Q

Th 17 cells play a critical role in mucosal and oral immunity. They protect barriers and induce inflammation when needed. What are the two interleukins they release? What do they do?

A

IL-17 and IL-22

Regulate tight junction protein expression (maintain barriers)

Induce antimicrobial peptide production (B-defensins, cathelicidins, lactoferrin)

Induce neutrophil chemotaxis

142
Q

Impaired or excessive Th17 function is linked to oral disease. What are they linked to?

A

Impaired Th17 function -Chronic mucocutaneous candidiasis (persistent fungal infection, deficient IL-17 signaling. Caused by deficient IL-17 receptors, impaired TH17 differentiation or development)

Excessive Th17 function - periodontitis (chronic and excessive neutrophil recruitment, chronic inflammatory cytokine production, osteoclast activation)

143
Q

What are 4 important roles that immunoglobulin secretion plays in mucosal membranes? What is the main Ig involved?

A

Neutralize pathogens/toxins

Bind/neutralize antigens in endosomes

Export toxins/pathogens from lamina propria to be secreted

Transported through M cells to a DC to shape microbiome

Predominantly IgA

144
Q

Mucosal antigens are constantly browsed by what three mechanisms? What is the outcome?

A

Antigen capture by macrophage

Uptake by goblet cell

Capture by interepithelial dendritic cell

Impacts IgA and antimicrobial peptide production and release

Commensal bacteria repress immune response

Pathogenic bacteria trigger immune response

145
Q

What are the three mechanisms in which mucosal antigens are constantly browsed by cells?

A

Nonspecific transport across epithelium (M cells)

FcRn-dependent transport

Apoptosis-dependent transfer

146
Q

Mucosal epithelial cells are active immune components. How? (6 things)

A

Actively direct immune responses

Express TLR and NOD receptors

Form inflammasomes

Phagocytose mucosal bacteria

Express cytokines and antimicrobial peptides

Induces local immune respsone

147
Q

Explain how epithelial damage can promote mucosal inflammation

A

Antibiotics kill commensal bacteria. Clostridium gains a foothold and produces toxins that causes mucosal injury.

Neutrophils and RBCs leak into gut between injured epithelial cells

This leads to pseudomembranous colitis

148
Q

Established pathogens illicit inflammatory responses. After pathogen evades mucosal immunity, what happens?

A

Local macrophage and DCs are activated

Leads to neutrophil recruitment

Th17 and Th1 response

149
Q

Gamma delta T cells are located in which layer of the mucosa?

A

Epithelial layer

Host and Defense (17 decks)

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