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Immunology Jenny > 10. Immune response in infections, mucosal immunity > Flashcards

10. Immune response in infections, mucosal immunity Flashcards

1
Q

Mechanisms of tissue damage by pathogens

A

Direct

  • Exotoxin (e.c pathogens)
  • Endotoxin (intravesicular pathogens)
  • Direct cytopathic effect (viruses)

Indirect

  • Immune complexes
  • Anti-host Ab
  • Cell-mediated immunity
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2
Q

Immune response is modulated by

A

1) Feature of pathogen (tissue specificity)
- EBV: B-cell (CR2)
- HIV: Macrophage, Th chemokine R
2) Entry
- SALT: skin associated lymphoid tissue
- MALT: mucosa -||-

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3
Q

Mucosal tissues of the human body

A
  • Respiratory tract
  • GI tract
  • Urogenital tract
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4
Q

External physical and biochemical protective mechanisms

A

Skin and mucosal surfaces:

  • Tight junctions
  • Ciliary movement
  • Stream of air/fluid
  • pH
  • Antibacterial molecules, defensins
  • Commensal bacteria in gut
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5
Q

pH in different parts of body

A
  • Skin: 5.5
  • Stomach: 1.2-3
  • Vagina: 4.5
  • Pancreas: 8
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6
Q

MALT
NALT
GALT

A
  • Mucosa associated lymphoid tissue
  • Nasopharynx -||-
  • Gut -||-
  • meeting points between lymphocyte-antigen
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7
Q

GALT

A

Gut associated mucosal tissue

  • Tonsils, appendix, Peyer’s patches
  • 2/3 of Ig production in body
  • Main task: complete exclusion of infectious agents and other Ag’s in intestinal lumen, local/systemic response, induction of tolerance
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8
Q

Components in mucosal immunity in gut

A

1) Cells: T- and B cells, langerhans cells, interstitial DCs, eosinophils, basophils, mast cells
2) Physical barrier: epithelial tight junctions
3) Stimulation of mucosal adaptive response
4) Transport of bacteria: M cells (sends microbes/partcles from gut lumen to lamina propria for interaction with immune cells - APC -> T- and B cell activation)

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9
Q

Peyer’s patch location + components

A

Loc: small intestine, bronchi, nasal mucosa
Components:
- M cells: Ag transport across epith
- SED (subepithelial dome): DC transports Ag to T cell zone
- TDA (T-dep area): T cells around follicles of B cells
- Afferent venules (HEV), efferent lymph vessels

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10
Q

M cells

A

“Microfolded”
- In epith above Peyer’s patches
- Function: take up Ag from lumen (endo-/phagocytosis)
and transport in vesicles to DC in lamina propria

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11
Q

DC cool function

A

Can extend processes across epith layer to grab Ag from the gut

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12
Q

Intestinal lymphocytes organization

A

1) Scattered lymphoid cells
- LPL: lamina propria lymphocyte
- IEL: intraepithelial lymphocytes
2) Organized lymphoid tissues
- Peyer’s patches
- Lymph follicles

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13
Q

Lamina propria cells + Ig

A
  • CD4 T cell (α4:β7 integrin, CCR9)
  • Macrophage
  • Mast cells
  • DCs
  • IgA
  • Plasma cell
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14
Q

Intraepithelial lymphocytes

A
  • CD8 T cell (αE:β7 integrin, CCR9)

- (γδ T, NKT cells)

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15
Q

Lymphocyte circulation within mucosal lymphoid system

A

Mucosal tissue => lymph => circulation => mucosal tissue

- E.g: Peyer’s patches => mesenteric lymph node => thoracic duct => circulation => mucosal tissue

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16
Q

GALT: two functional sites

A

1) Inductive site: Peyer’s patch
- Take up antigen through M cells->APC-> B/T cell
- >lymph node->thoracic duct->circulation
2) Effector site: Immune exclusion (SIgA/SIgM)
* Se bilde

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17
Q

Intraepithelial lymphocyte function

A

CD8 T cell
- Virus infect mucosal epith cell -> infected cell display viral peptide to CD8 via MHC I -> activated IEL (CD8) kills infected cell by perforin/granzyme and Fas-dependent pathways

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18
Q

Humoral immunsystem of mucosa

A

IgA-dominated

  • IgM/IgA isotype switch: generated in mucosa
  • Active, receptor-mediated transport: IgA dimer+IgM polymer
  • Passive, paracellular diffusion: IgG and IgA monomer
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19
Q

IgA promoting cytokines

A

IL-5, IL-2 and TGF-β

20
Q

TD- vs TI-class switching mucosal B cells

A

TD: T cell dependent
- DC (TGF-β, NO + costimulation w/CD40L from Th
- Differentiate into high affinity IgA producing plasma cell
TI: T cell independent (First line of defence!)
- Activated only by DC (APRIL; BAFF; TGF-β)
- Differentiate into low-affinity B1 cell, which can further differentiate into IgA producing plasma cell

21
Q

Secretory IgA function + mechanism of secretion

A

Function:

1) Can bind and neutralize pathogens and toxins
2) Bind and neutralize Ag’s internalized in endosomes
3) Export toxins and pathogens from lamina propria to lumen while being secreted

Mechanism: IgA binds to poly-Ig R on basolat surface of epith cell -> endocytosis + transcytosis to apical surface -> release IgA dimer+secretory component to lumen

22
Q

Commensal microorganisms

A

Microorganism that resides in body, but doesn’t cause harm

  • Human intestine: 10^4 bacteria
  • Benefit: compete with pathogenic bacteria for food++
23
Q

E.coli benefit for host

A

Vitamin producer, especially vitamin K

24
Q

Intestinal bacteria location and diversity

A

Increasing numbers and diversity from the duodenum towards the colon

25
TLR location gut epith cells
Intracellularily and on basolat surface
26
Immune checkpoints for scaling microbial treath
1) First checkpoint: soluble or particulate PAMPs? - Pro-inflammatory (IL-6, IL-12, TNF) 2) Second checkpoint: dead or alive? - Viable: Vita-PAMP -> NLRP3 inflammasome activation - > induces IL-1β production 3) Third checkpoint: pathogen or not? - Cell death and barrier disruption * Se bilde 4) Fourth checkpoint: harmless colonization or harmfuk invasion? - NLR: detect 'activity' of virulence factors such as toxins or secretion systems
27
Inflammasome
Regulate the activation of caspase-1 and induce inflammation in response to infectious microbes and molecules derived from host proteins - Caspase 1 activates IL-1β and IL-18 - Components of inflammasome: NLRP3, ASC, pro-caspase 1
28
Salivary microbiome important bacteria
- Porphyromonas gingivalis (In periodontitis of gums, plaque accumulation) - Fusobacterium nucleatum (naturally present, in dental plaque) - (Streptococcus) - (Prevotella)
29
Porphyromonas gingivalis lead to chronic disease
1) Can get citrullinated -> citrullinated proteins can be recognized by ACPA (anti-citrullinated peptide Ab) - ACPA is prod from TD- B cells (T cell activation happens in genetically susceptible individuals as response to danger signals) - ACPA can also recognize citrullinated joint proteins - ACPA-antigen complexes (joint+bacteria) -> perpetuation of inflammatory reaction -> chronic RA 2) Also plays a role in atherosclerotic plaque
30
Fusobacterium nucleatum protection from P. gingivalis
F. nucleatum cellwall factor promotes β defensin expression | - F. nucleatum resistant against β defensins, P. gingivalis is not
31
How immune system decides which mechanism is best to remove pathogens
3 decision level: - Size - Localization - Lifestyle (metabolic property)
32
Pathogen size effect on immune response
1) Smaller than phagocyte: Intracellularily killing (mainly) - > no collateral damage 2) Bigger than phagocyte: Extracellular killing (degranulation) - Neutrophils+eosinophils: basic molecules - Basophils: acidic molecules
33
Effector mechanisms to extracellular macroparasites (bigger than phagocyte) overview
1) Barrier functions: intact skin, mast cells (induce wash out of bacteria - diarrhea, cough etc) 2) Eosinophils+basophils: degranulation (E: basic, B: acidic) 3) Th2 induced ADCC * Damage of parasite by lysosomal enzymes, basic proteins (MBP) and nitrogen oxides
34
Effector mechanisms to e.c macroparasites detailed
1) Basophils prod IL-4+IL-5 -> LN: Th2 cells arise 2) Th2 cells: B cells -> plasma cells 3) IL-4: class switch to IgE 4) IL-5: activation of eosinophils 5) IgE opsonize the parazite 6) Basophils and eosinophils activated for more degranulation
35
Localization of pathogens
1) Intracellular - Vesicular (lysosome-endosome) - Cytoplasmic 2) Extracellular - On body surface - In extracellular fluid
36
Examples of intracellular bacteria
Vesicular: Mycobacterium leprae and Plasmodium falciparum Cytoplasmic: Influenza and Listeria
37
Examples of extracellular bacteria
S. pneumoniae Trypanosoma brucei Ascaris
38
Mechanism based on localization
1) E.c free Ag: Humoral immunity (Ab prod, TI) 2) Phagocytosed e.c Ag MHC II: Ab prod, TD 3) Intracellular: no humoral immunity
39
Effector mechanisms to extracellular bacteria
1) Humoral (Ab+complement) - Neutralization - Opsonization and Fc-R mediated phagocytosis - Phagocytosis of C3b-coated bacteria - Inflammation - Lysis of microbe 2) T-cell dependent - Inflammation (IL-17, TNF, other cytokines) - Macrophage activation (IFNγ) - Antibody response (various cytokines
40
Pathogen lifestyle
Virus: no own metabolism - use metabolism of cell - Presented by MHC I Bacteria (i.c): phagocytosed, in lysosomes - Presented by MHC II
41
Effector mechanism to viruses
Innate immunity 1) Infected cell produce IFNα,β => Increased MHC I and NK activity (prevent spreading - antiviral state) 2) NK cell killing Adaptive immunity 3) Lymph node: IL-12 from DC => Th0->Th1, which can activate/promote proliferation of Tc and NK cells (?) 4) Cytotoxic killing (Tc) 5) Lymph node: B cell endocytosis? + generation of Ab 6) Neutralization by Ab's
42
Effector mechanisms to intravesicular pathogens and unicellular protozoans
I.c pathogens survive in macrophages - protected against i.c killing - PRR DC move to LN => secretes IL-12 => Th0->Th1 => Th1 move to infection site+secrete IFNγ => activates macrophage to kill engulfed pathogen (nitrogen, oxygen radicals)
43
Effector mechanisms to kill i.c cytoplasmic pathogens
CD8 CTL (activated by Th1 cell)
44
Escape mechanisms of parasites
1) Low antigenicity: high rates of mutation 2) Hiding: i.c or in lumen 3) Antigen masking: cover itself with host antigens 4) Capsule formation 5) Molecular mimicry: e.g hyaluronic acid 6) Inhibition of opsonization: e.g protein A 7) Proteolytic cleavage of Ab's: e.g IgA protease
45
How pathogens avoid phagocytosis
1) Activate apoptosis 2) Inhibition uptake/inactivating complement 3) Inhibition of signal transduction 4) Escape from endosomes/disruption of phagosome membrane->cytoplasm 5) Prevent fusion of phagosomes and lysosomes 6) Inhibit processing (e.g inactivate reactive oxygen and nitrogen species)
46
How pathogens avoid adaptive immune response (only main points)
1) Stimulate prod of immunosuppressive cytokines (!) 2) Decrease MHC I and II expression 3) Activation of inhibitory signals 4) Activation of Treg

Immunology Jenny (16 decks)

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