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HDM > Final Exam- Week 3 > Flashcards

Final Exam- Week 3 Flashcards

1
Q

mucosal barrier

A

External environment interface: lots of immune cells

neutrophils, MPs, T cells (h and c), eosinophils, mast cells, DCs, B cells, plasma cells

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2
Q

GALT

A 
Gut-ass lymphoid tissue
Microvillar extensions: actin-rich
Epithelial cells: tight junctions
Secreted mucins-> glycocalyx
Paneth cells-> antimicrobial peptides
M cells: over Peyer's patches/follicles for luminal microbe sampling (reduced mucin secretion)
SED: pro-APCs
DCs: extend dendrites b/w tight junctions for luminal microbe sampling
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3
Q

glycocalyx

A

part of GALT

formed by attached and secreted mucins on apical side of epithelial cells

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4
Q

Paneth cells

A

secrete antimicrobial peptides in crypts

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5
Q

M cells

A

microfold cells over Peyer’s patches and follicles in GALT
help sample luminal microbes
reduced mucin secretion and modified apical/basolateral surfaces to inc uptake/transport of luminal contents

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6
Q

SED

A

Sub-epithelial dome of Peyer’s patches and lymphoid follicles
contains dendritic cells

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7
Q

dendritic cells (GALT)

A

can extend dendrites between tight junctions to sample luminal contents (microbes)

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8
Q

Th cells (Ag recognition in gut)

A
  1. Ag enters through M cells -> DCs
  2. DCs -> T cells (Peyer’s Patch) or -> mesenteric LN
  3. activated T cells disperse through peripheral imm sys (efferent lymph vessel-> thoracic duct-> bloodstream-> lamina propria)
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9
Q

Anti-inflammatory mechanisms (gut)

A
  1. Immune Exclusion: limit pathogen colonization (IgA)

2. Oral Tolerance: food proteins/microbiota suppress Th1 (IgG), Th2 (IgE), Th17 (IL-17)

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10
Q

Immune Exclusion

A

anti-inflammatory mechanism in the gut (few days)
limits pathogen colonization by IgA secretion (some IgM)
Mechanism:
1. Ag recognition at inductive site (PP)
2. Stimulation of T (CD4/8) and B (IgA/M) cells at effector site (mucosa)

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11
Q

Oral Tolerance

A

anti-inflammatory mechanism in the gut

food proteins/microbiota (TGFb)-> Treg diff-> suppress inflammatory rxns from Th1 (IgG), Th2 (IgE and DTH), Th17 (IL-17)

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12
Q

Treg cells (GALT)

A

up to 10%

suppress Th1, Th2, and Th17 cells in oral tolerance

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13
Q

Th17 cells

A

accumulate in intestine, possibly due to segmented filamentous bacteria (SFB)
autoimmune disease: produce IL-17 and IL-22 (pro-inflam)

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14
Q

Treg cells

A

subset of CD4+ cells, CD25+ (have IL-2 receptor)
Transcr factor: FOXP3
accumulate in intestine (number likely controlled by microflora), prevent self-reactive imm resp against microflora
depletion-> Th cell expansion (removes suppression)-> intestinal inflammation

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15
Q

IgA

A 
secreted as SIgA due to J subunit
promotes intestinal barrier function
maintains commensal mutualism
coats bacteria (commensal AND pathogenic) to inhibit binding to host epithelium/penetration of lamina propria
regulates composition/function of gut microflora
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16
Q

flagellin

A

microflora-derived

promotes synthesis of retinoic acid-> facilitates differentiation of IgA B cells

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17
Q

microflora

A 
maintain homeostasis in GI
maintain Treg cells and IgA production
develop GALT
prevent pathogenic colonization
polarize imm responses (regulate own composition)
digest/ferment carbs
conjugate bile acids
produce vitamins
18
Q

IgA deficiency

A

most common immunodeficiency
compensated for by other Ig’s
usually not discovered until genetic testing

19
Q

environmental signals

A

control balance b/w tolerance and proinflammatory responses

20
Q

Functional medicine

A

studies how commensal microflora affects different aspects of health (ex- asthma)
treat ex- clean out microflora, replace w/healthy colonization

21
Q

germ-free mice

A

show decreased mucus thickness
longer/thinner villi
less complex vascular network
shallower crypts w/less proliferative stem cells
few lymphoid follicles, immature PPs/MLNs
low IgA and antimicrobial peptides

22
Q

microflora protection

A 
GALT development
inc Th17/Th1
inc barrier fxn
inc anti-microbial peptides
Beneficial bacteria: inc Treg, inc IL-10, inc anti-microbial peptides
23
Q

REGIIIg

A

anti-microbial peptides

inc by commensal microflora

24
Q

Chronic inflammation

A

due to environment and genetics -> dysbiosis
very high Th17/Th1
dec Treg/IL-10/anti-microbial peptides

25
Q

microflora and NFkB

A

commensal microflora SUPPRESS NFkB (so anti-inflam)

26
Q

Macrophage microflora tolerance

A

don’t sense microflora -> don’t secrete pro-inflam CKs
prevents chronic inflammation in mucosa
(microflora suppress NFkB)

27
Q

commensal Bacteroides

A

Prevents inflammation by creating complex w/NFkB
Increases proinflam response caused by S. Enteritidis
Induces PPAR-> exports activated NFkB from nuc

28
Q

Absence of commensal bacteroides

A
  1. Salmonella flagellin binds TLR5 on intestinal epithelial cells
  2. Activates IkB kinase (IKK)-> activ/nuc translocation of NFkB
  3. NFkB transcribes pro-inflam genes
29
Q

Hyperimmunity

A

Over production of pro-inflam mediators (IL-6, IL-12, TNF)

30
Q

Immunodeficiency

A

Mutations in immuno-regulatory proteins such as NOD2 or IL-10 influence gut microbiota composition

31
Q

NOD2

A

Nucleotide-binding oligomerization domain protein 2
Involved in immuno-regulation
Mutated in immunodeficiency

32
Q

Factors shaping intestinal microbial composition

A

Lifestyle (exercise, diet- bacteria like FIBER)
Hygiene
Abx
Hyperimmunity/Immunodeficiency

33
Q

Can prescribe w/Abx

A

Probiotic (yogurt)
Every 6-12 hrs AFTER abx
NOT AT SAME TIME

34
Q

Dysbiosis

A

Altered intestinal microbiota

Linked to chronic inflammation and metabolic dysfunction

35
Q

Chronic inflammatory diseases

A

IBS
Asthma
Arthritis, Obesity, CV disease

36
Q

Central tolerance

A

Induced in IMMATURE self-reactive lymphocytes
Location: bone marrow & thymus
Fxn: Prevents MATURATION of self-reactive lymphocytes
Not perfect-> peripheral tolerance as back up to prevent activation

37
Q

Peripheral tolerance

A

Induced in MATURE self-reactive lymphocytes
Location: peripheral sites
Fxn: prevents ACTIVATION of self-reactive lymphocytes
(Treg cells watch over)

38
Q

Central T cell Tolerance

A
  1. Thymus: Thymic Epithelial Cells present self Ag to Immature T cells
  2. Cells w/TCRs w/no affinity for self Ag-self MHC -> no survival signal-> spontaneous apoptosis in thymus
    Cells w/TCRs w/high affinity for self Ag-MHC -> death signal -> apoptosis
    Cells w/TCRs w/INTERMED affinity for self Ag-MHC -> MATURE in thymus-> MIGRATE to periphery-> activated
39
Q

AIRE

A

AutoImmune REgulator gene (possibly a transcr factor)
Expressed in thymic epith cells
Exposes imm cells to complete set of self-Ags

40
Q

AIRE mutation

A

Mutation-> decreased expression of self-Ags in thymus-> imm cells not exposed to complete set of self-Ags-> breaks central tolerance-> Autoimmune Polyendocrine Syndrome (APS): Abs/lymphocytes destroy endocrine organs

41
Q

Thymic epithelial cells

A

Self-APCs
Express large number of self-Ags, present to developing T cells
AIRE (TF) enables them to activate tissue-restricted Ags (TRAs)
Mutation-> dec expression of self-Ags

42
Q

TRAs

A

Tissue-restricted Ags
Genes activated in thymus by AIRE in thymic epith cells-> peptides displayed on Medullary Thymic Epithelial Cells
Self-reaction w/TRA by T cell-> neg selection (deletion)
AIRE mutation-> TRA-reactive T cells not tested-> not eliminated (failure of neg selection)-> enter periphery-> autoimmunity (like APS)

HDM (6 decks)

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