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Y Immunology > Lecture 8: Mucosal Immunity (Ben) > Flashcards

Lecture 8: Mucosal Immunity (Ben) Flashcards

1
Q

What are some physical + biochemical barriers for pathogen penetration in the mucosa?

A
  1. Tight Junctions
  2. Ciliary Movement - in trachea
  3. Fluid/Air Movement - coughing, sneezing, etc.
  4. pH - unfavorable for pathogens
  5. Antibacterial molecules - (details in later card)
  6. Commensal flora
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2
Q

What are the pH values of the…

skin?

stomach?

vagina?

pancreatic juice?

(prob not super important)

A
  • skin 5.5
  • stomach 1.2-3.0
  • vagina 4.5
  • pancreas 8.0
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3
Q

What antibacterial molecules can be found in…

saliva/colostrum? tears, sweat + saliva?

others?

A
  • lactoperoxidase in saliva/colostrum
  • lysozyme in tears, sweat + saliva
  • defensins - in many body fluids/tissues
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4
Q

Give some examples of GALT.

Large proportions of what cell types + molecules are found in it?

What are its 3 ‘tasks’?

A
  • Peyer’s patches, tonsils, appendix
  • more lymphocytes than elsewhere; 2/3 of total Ig
  • Tasks: exclude pathogens/antigens from invasion; initiate local/systemic immune responses; induce tolerance
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5
Q

Describe the structure of a Peyer’s patch from luminal to basal.

A
  • M cells at lumen
  • SED - “subepithelial dome” = APCs
  • TDA - T cells below SED, surrounding follicles
  • Follicles - clusters of B cells within TDA
  • afferent lymph vessels connect the most basal parts of the patch to nearby mesenteric lymph nodes
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6
Q

Describe the function of M cells in the intestine.

A
  • transport antigens across the epithelium to dendritic cells below
  • (take up luminal antigen via endo-/phagocytosis -> transport it basally in vesciles -> release it to subepithelial layer where dendritic cells are)
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7
Q

How can T cells be categorized by location in mucosal immunity?

A
  • can be “scattered” as effector cells or “organized” in Peyer’s patches and isolated follicles as immune response inducers
  • scattered T cells can be intraepithelial (IPL) CD8+ cells or lamina propria (LPL) CD4+ cells
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8
Q

What are the two “functional sites” of GALT?

A
  • Inductive Site - Peyer’s patches + isolated follicles in which T/B cells are activated + then travel through lymph + blood back to…
  • Effector Site - T cells enter epithelium/lamina propria; B cells enter lamina propria + secrete mostly IgA and some IgM
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9
Q

Describe intraepithelial lymphocytes (IPLs).

How many are there? What kinds of T cells?

A
  • 10-20 IPLs per 100 epithelial cells
  • many CD8+ T cells
  • 50% gamma-delta T cells, many NKTs as well
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10
Q

Describe the effector function of an intraepithelial CD8+ cell with regards to viral infection.

A
  • virus in lumen infects epithelial cell (e.g. enterocyte)
  • infected cell presents viral peptide via MHC-I
  • CD8+ cell uses Perforin/Granzyme and FasL mechanisms to kill the infected cell
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11
Q

How does transepithelial transport of antibodies from lamina propria to the lumen differ when the Abs are in monomeric vs. polymeric forms?

A
  • IgA dimers + IgM pentamers transported via active receptor-mediated transport
  • IgA/IgM monomers transported via passive paracellular diffusion
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12
Q

What cytokines are involved in differentiation of B cells into IgA-secreting plasma cells?

A
  • IL-5
  • IL-2
  • TGF-B
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13
Q

How does T-dependent class switching to IgA take place in the mucosa?

What is the affinity of the resutling IgA

A
  • M cells transport antigens to Peyer’s patch DCs
  • DCs activate naive T cells -> CD4+ Th
  • Th cells stimulate B cells with their CD40L + nearby dendritic cells provide TGF-B co-stimulation to induce class switch
  • resulting plasma cell secretes high affinity IgA
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14
Q

How does T-independent class switch to IgA work in mucosal immunity?

What is the affinity of the resulting IgA?

How does the timescale of this class switch mechanism differ from T-dependent?

A
  • PAMPs bind to TLR on APCs + activate them
  • APCs secrete TGF-B + other cytokines which induce class switch of B-1 cells to IgA plasma cells
  • resulting IgA is low affinity
  • is a faster class switch via innate immunity mechanisms, acting as a “first line defense”
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15
Q

How is IgA transported from the lamina propria to the lumen of mucosal organs?

A
  • binds to polyIg receptor basolateral epithelium
  • is endocytosed into a vesicle
  • transcytosis to apical face of epithelium
  • releases into lumen along with secretory component of the receptor
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16
Q

What are three locations in the mucosa where IgA can function?

A
  1. Luminal mucus layer - bind/neutralize pathogens + toxins
  2. Intracellular endosomes - neutralize antigens
  3. Lamina propria - export toxins/pathogens from LP to lumen
17
Q

Where are TLRs located in relation to gut epithelium?

A
  • on basolateral surface + intracellularly in endosomes
18
Q

What 5 “checkpoints” are there in the mucosa for determining whether to induce an immune response + what response to induce?

(this is a very vague classification system used in the ppt)

A
  1. Soluble vs. particulate PAMPs
  2. Dead vs. Alive - is microbe viable?
  3. Pathogen vs. Non-Pathogen - virulence detection
  4. Harmless Colonization vs. Harmful Invasion
  5. Regulatory vs. Inflammatory response
19
Q

What pro-inflammatory cytokines are produced immediately upon recognition of PAMPs in mucosal immunity?

(this is info from some very vague slides that I’m not really sure how to study)

A
  • IL-6
  • IL-12
  • TNF
20
Q

What are the signs of microbial viability called?

What kind of response do they induce?

An example of one?

A
  • “vitaPAMPs” such as prokaryotic mRNA
  • via PRRs such as NLRP3 they induce inflammasome activation + production of IL-1B
21
Q

What receptors are useful for detecting the “activity” of virulence factors such as exotoxins + secretion systems?

A

NLRs

nod-like receptors

22
Q

Give an example of a way in which invasiveness vs. commensal tendency is determine in mucosal immunity.

(specific microbe + changes btwn invasive/harmless form)

(not sure how important this is…)

A
  • C. albicans can transform from an inocuous yeast to invasive hyphal form
  • hyphal form expresses B-glucans which are recognized by PRRs (TLR2 + Dectin 1) on immune cells
23
Q

What potentially harmful salivary commensal was mentioned in the lecture?

What diseases is it associated with + how?

A
  • P. gingivales
  • associated with periodontitis, RA + atherosclerosis
    • in RA -> citrullinated bacterial proteins are bound by Abs and deposited immune complexes cause arthritis
24
Q

What other oral commensal prevents invasion by P. gingivales + how?

A
  • F. nucleatum - has a cell wall factor which promotes beta-defensin expression which harms P. gingivales
25
Q

How does size of a pathogen affect how the immune system responds to it?

A
  • smaller than phagocyte -> pathogen is phagocytosed + killed intracellularly; usually via neutrophils; no collateral damage involved
  • larger than phagocyte -> induces degranulation + extracellular killing by neutro-/eosino-/basophils; some collateral damage involved
26
Q

What are 3 mechanisms for dealing with extracellular macroparasites such as worms?

A
  • Barrier Functions: skin blocks penetration; mast cells induce diarrhea/coughing to expel parasite
  • Degranulation: eosino-/basophils secrete toxins
  • ADCC: Th2 cells induce cytotoxicity
27
Q

What two cytokines are important in dealing with extracellular macroparasites + how?

A
  • IL-4 - induces IgE class switching -> IgE opsonizes parasite
  • IL-5 - activates eosinophils which bind IgE via FcERI, degranulate + attack parasite with MBP, lysosomal enzymes + NO
28
Q

What are 3 possibilities for the location of a pathogen in relation to the cell?

Examples of each (less important)?

A
  • Intracellular Vesicular - in lyso-/endosome
    • M. leprae + P. falciparum (malaria)
  • Intracellular Cytoplasmic - Influenza / Listeria
  • Extracellular - S. pneumo / Trypanosoma / Ascaris
29
Q

How does antigen location affect what kind of antibody production is elicited?

A
  • Free Extracellular Ag - induces humoral immunity (Ab production) in T-independent manner
  • Extracellular Ag Presented via MHC-II - induces T-dependent Ab production
  • Intracellular - no humoral immunity
30
Q

How do the metabolic properties of intracellular pathogens affect what kind of immune response it elicits?

(in .ppt this is referred to as “lifestyle” of the pathogen… a weird wording i wouldn’t be surprised to see in an mcq)

A
  • Viruses - don’t have their own metabolism; use infected cells metabolism; elicit MHC-I presentation -> cytotoxic response
  • Intracellular Bacteria - enter macrophages via phagocytosis; are in lysosomes within cell; presented via MHC-II
31
Q

How does a graph of innate immune mechanisms + adaptive immune mechanisms + virus titer vs. time look?

A
  • Innate: IFN-alpha/beta come first + peak around day 2; NK cells act next + peak day 4
  • Adaptive: CTLs plateau days 7-11; antibodies rise day 5-10 then slowly fall
  • Virus titer: rises slowly day 0-5, then falls til gone day 12
32
Q

Describe effector mechanisms for immune reactions against viruses.

A
  1. Infected cells release TNF-alpha/beta -> increases MHC-I expression and…
  2. NK cell activity
  3. Dendritic cells secrete IL-12 to stimulate Th1 differentiation
  4. Th1 cells stimulate Tc and NK cytoxocity
  5. Nodal B cells endocytose viruses + generate Abs
  6. Abs + complement -> viral neutralization
33
Q

How does interferon work against viral infections?

A
  • binds to an interferon receptor on host cells
  • induces antiviral proteins that bind to and inhibit the viral genome –> inhibited viral replication
34
Q

Describe a response against intravesicular pathogens or unicellular protozoans.

A
  • intracellular pathogens often avoid intracellular killing + can survive in macrophages
  • in lymph nodes, after activation via PRRs, DCs secrete IL-12 to induce Th1 differentiation
  • Th1 cells then reinforce phagocytes by secreting IFN-y which increases nitrogen + oxygen free radicals in their phagolysosomes
35
Q

Name some “escape strategies” of parasites.

(this slide said “not to be recognized” which i guess means we don’t need to learn it… who knows)

A
  • Low antigenicity - mutations -> less antigenic proteins etc.
  • Intracellular “hiding”
  • Antigen masking - covers its antigens with host antigens
  • Capsule formation
  • Molecular mimicry - HA in S. pyogenes capsule
  • Opsonization inhibiton - S. aureus protein A
  • Ab cleavage - as in IgA-proteases
36
Q

What are 6 mechanisms for pathogenic avoidance of phagocytosis?

(again not sure how important)

A
  1. Activating apoptosis of the phagocyte
  2. Inactivate complement
  3. Inhibit signal transduction - CMV inhibs IFN signaling
  4. Escapse from endo/phagosome - trypanosoma
  5. Prevent phagolysosome formation - toxoplasma
  6. Inhibition of processing - M. leprae inactivate ROS
37
Q

Name 4 mechanisms pathogens use to disturb adaptive immune respones.

(slide had 10 but these 4 were highlighted)

A
  1. Stimulate immunosuppressive cytokine production
  2. Decrease MHC expression - adenovirus secretes protein that keeps MHC in ER
  3. Activation of inhibitory signals
  4. Activation of Tregs - via IL-10 and TGF-B

Y Immunology (18 decks)

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