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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
Q

TLR location gut epith cells

A

Intracellularily and on basolat surface

26
Q

Immune checkpoints for scaling microbial treath

A

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
Q

Inflammasome

A

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
Q

Salivary microbiome important bacteria

A
  • Porphyromonas gingivalis (In periodontitis of gums, plaque accumulation)
  • Fusobacterium nucleatum (naturally present, in dental plaque)
  • (Streptococcus)
  • (Prevotella)
29
Q

Porphyromonas gingivalis lead to chronic disease

A

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
Q

Fusobacterium nucleatum protection from P. gingivalis

A

F. nucleatum cellwall factor promotes β defensin expression

- F. nucleatum resistant against β defensins, P. gingivalis is not

31
Q

How immune system decides which mechanism is best to remove pathogens

A

3 decision level:

  • Size
  • Localization
  • Lifestyle (metabolic property)
32
Q

Pathogen size effect on immune response

A

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
Q

Effector mechanisms to extracellular macroparasites (bigger than phagocyte) overview

A

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
Q

Effector mechanisms to e.c macroparasites detailed

A

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
Q

Localization of pathogens

A

1) Intracellular
- Vesicular (lysosome-endosome)
- Cytoplasmic
2) Extracellular
- On body surface
- In extracellular fluid

36
Q

Examples of intracellular bacteria

A

Vesicular: Mycobacterium leprae and Plasmodium falciparum
Cytoplasmic: Influenza and Listeria

37
Q

Examples of extracellular bacteria

A

S. pneumoniae
Trypanosoma brucei
Ascaris

38
Q

Mechanism based on localization

A

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
Q

Effector mechanisms to extracellular bacteria

A

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
Q

Pathogen lifestyle

A

Virus: no own metabolism - use metabolism of cell
- Presented by MHC I
Bacteria (i.c): phagocytosed, in lysosomes
- Presented by MHC II

41
Q

Effector mechanism to viruses

A

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
Q

Effector mechanisms to intravesicular pathogens and unicellular protozoans

A

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
Q

Effector mechanisms to kill i.c cytoplasmic pathogens

A

CD8 CTL (activated by Th1 cell)

44
Q

Escape mechanisms of parasites

A

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
Q

How pathogens avoid phagocytosis

A

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
Q

How pathogens avoid adaptive immune response (only main points)

A

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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