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Lernmaterialien für Immunologie B an der Universität Wien

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Germ-free parts of the human body

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Liver 

Spleen 

Bones 

Muscles 

Blood

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Cells of the intestenal epithelium

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Enterocytes: secrete anti-microbial proteins Paneth cells: specialized epithelial cells in the ileal crypts, produce abundant anti-microbial compounds such as α- defensins to regulate bacterial populations 

Goblet cells: produce mucin glycoproteins, constituents of the mucus layer, where antimicrobial proteins are enriched and resistance against bacteria is enforced. 

Peyer's patches: Sampling of bacterial products by dendritic cells (DCs) through their dendrites or by M-cells via transcytosis leads to antigen presentation to the lymphocytes in Peyer's patches. This results in the development of plasma cells, which produce and secrete IgA into the luminal surface of the intestine.

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What happens at a immuotherapie?

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The cancer immunotheraies anti-CTLA4 and anti-PD1 remove certain natural barriers to immune activity.

anti-CTLA4: allows tumor-fightig cells to multiply

anti-PD1: blocks a molecule that shields tumor cells from attack


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Which properties have iDC?

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  • Sample the lumen
  • Loaded with food proteins -iDCs promote peripheral tolerance of B and T cells
  • Poor biocidal activity
  • Short lifespan
  • Constitutively produce RA
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What are the functions of the normal flora?

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  • Competition with pathogenic microorganisms 
  • Control of the balance between tolerance and promotion of the immune response 
  • Maintenance of the immunological barrier 
  • Host-specific maturation of the gut immune system (through bacteria AND VIRUSES)
  • Co-determined by the host‘s genetics
  • Promotes systemic non-specific immunity
  • Prevents allergy
  • Promotes the development and maintenance of the blood-brain barrier
  • May promote neurodegeneration
  • Impact on metabolism
  • Interaction with drugs
Lösung ausblenden
TESTE DEIN WISSEN

How does the gut flora interact with drugs?

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  • Irinotecan (CPT-11) (used in the administration of cancer) is administered iv as a prodrug 
  • Tissue - CE (Carboxylesterases) convert it into cytotoxic SN-38 (active drug, kills cells; mostly cancer cells, but not only) 
  • Liver UGTs (Uridine diphosphoglucuronosyltransferases) inactivate SN-38 converting it into the non-toxic SN38G, excreted in the gut via the bile 
  • β-glucuronidases (β-gluc) produced by gut flora metabolize SN-38G to SN-38 
  • β-gluc inhibitors diminish irinotecan gut toxicity
Lösung ausblenden
TESTE DEIN WISSEN

Who conditions iDCs to become tolerogenic?

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epithelial cell- derived factors

  • thymic stromal lymphopoietin (TSLP)
  • transforming growth factor-β (TGFβ) 
  • retinoic acid,
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Steps of infection?

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  • The microbe encounters its host (the microbe gets somehow in touch with the host the consequence can be that the microbe is immediately destroyed or the next step is colonialisation) 
  • Colonialisation (can still be without any disease) 
    • The microbe enters the host 
    • The microbe spreads in the host 
    • The microbe multiplies in the host 
  • The microbe damages the host 
  • End result
    • the host wins 
    • host and microbe coexist 
    • the microbe wins
Lösung ausblenden
TESTE DEIN WISSEN

How is the host damaged by the pathogen, which types of toxins are there?

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  • Cytolytic toxins (essentially lyse cells)
    • LIPASES (C. perfringens α-Toxin) 
    • PORE-FORMING TOXINS (S. aureus α-Toxin, Streptolysin O) (integrate into the host cell membrane and dissolve, host cell can leak out, leads to damage of the host cell (iron, wrong pH) 
  • Protein synthesis-inhibiting Toxins (Diphtheria Toxin) 
  • Pharmacologically active Toxins (Cholera Toxin) (changes the activity of enzymes) 
  • Neurotoxins (tetanospasmin, C. botulinum Toxin) (the central nervous system is damaged) 
  • Endotoxins
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TESTE DEIN WISSEN

On what depends virulence?

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=ability of the pathogen to cause damage, also factors to help the pathogen with colonizing the host 

Pathogen 

  • Invasion 
  • Toxicity 


Host 

  • General fitness 
  • Health status (chronic or acute diseases)
  • Immune status (chemo-radio patients, HIV) 
  • Extreme stress 
  • Age & gender 
  • Genetic factors
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TESTE DEIN WISSEN

What does dynamic virulence mean?

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Bacteria can evolve from non-pathogens to become pathogens through acquisition of new genetic material. Pathogenic bacteria can undergo further genetic modification that leads to altered virulence and changes in their genome.

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3 Types of re-emerging diseases

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1) Evolution of new strains within the same host species (methicillin-res S. aureus MRSA)

2) Switch to new host species (MRSA, HIV, SARS-CoV, covid-19 causing SARS--CoV-2)

3) Switch to new host species plus change in geographic range (West Nile virus in America)

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  • 102 Lernmaterialien

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Q:

Germ-free parts of the human body

A:

Liver 

Spleen 

Bones 

Muscles 

Blood

Q:

Cells of the intestenal epithelium

A:

Enterocytes: secrete anti-microbial proteins Paneth cells: specialized epithelial cells in the ileal crypts, produce abundant anti-microbial compounds such as α- defensins to regulate bacterial populations 

Goblet cells: produce mucin glycoproteins, constituents of the mucus layer, where antimicrobial proteins are enriched and resistance against bacteria is enforced. 

Peyer's patches: Sampling of bacterial products by dendritic cells (DCs) through their dendrites or by M-cells via transcytosis leads to antigen presentation to the lymphocytes in Peyer's patches. This results in the development of plasma cells, which produce and secrete IgA into the luminal surface of the intestine.

Q:

What happens at a immuotherapie?

A:

The cancer immunotheraies anti-CTLA4 and anti-PD1 remove certain natural barriers to immune activity.

anti-CTLA4: allows tumor-fightig cells to multiply

anti-PD1: blocks a molecule that shields tumor cells from attack


Q:

Which properties have iDC?

A:
  • Sample the lumen
  • Loaded with food proteins -iDCs promote peripheral tolerance of B and T cells
  • Poor biocidal activity
  • Short lifespan
  • Constitutively produce RA
Q:

What are the functions of the normal flora?

A:
  • Competition with pathogenic microorganisms 
  • Control of the balance between tolerance and promotion of the immune response 
  • Maintenance of the immunological barrier 
  • Host-specific maturation of the gut immune system (through bacteria AND VIRUSES)
  • Co-determined by the host‘s genetics
  • Promotes systemic non-specific immunity
  • Prevents allergy
  • Promotes the development and maintenance of the blood-brain barrier
  • May promote neurodegeneration
  • Impact on metabolism
  • Interaction with drugs
Mehr Karteikarten anzeigen
Q:

How does the gut flora interact with drugs?

A:
  • Irinotecan (CPT-11) (used in the administration of cancer) is administered iv as a prodrug 
  • Tissue - CE (Carboxylesterases) convert it into cytotoxic SN-38 (active drug, kills cells; mostly cancer cells, but not only) 
  • Liver UGTs (Uridine diphosphoglucuronosyltransferases) inactivate SN-38 converting it into the non-toxic SN38G, excreted in the gut via the bile 
  • β-glucuronidases (β-gluc) produced by gut flora metabolize SN-38G to SN-38 
  • β-gluc inhibitors diminish irinotecan gut toxicity
Q:

Who conditions iDCs to become tolerogenic?

A:

epithelial cell- derived factors

  • thymic stromal lymphopoietin (TSLP)
  • transforming growth factor-β (TGFβ) 
  • retinoic acid,
Q:

Steps of infection?

A:
  • The microbe encounters its host (the microbe gets somehow in touch with the host the consequence can be that the microbe is immediately destroyed or the next step is colonialisation) 
  • Colonialisation (can still be without any disease) 
    • The microbe enters the host 
    • The microbe spreads in the host 
    • The microbe multiplies in the host 
  • The microbe damages the host 
  • End result
    • the host wins 
    • host and microbe coexist 
    • the microbe wins
Q:

How is the host damaged by the pathogen, which types of toxins are there?

A:
  • Cytolytic toxins (essentially lyse cells)
    • LIPASES (C. perfringens α-Toxin) 
    • PORE-FORMING TOXINS (S. aureus α-Toxin, Streptolysin O) (integrate into the host cell membrane and dissolve, host cell can leak out, leads to damage of the host cell (iron, wrong pH) 
  • Protein synthesis-inhibiting Toxins (Diphtheria Toxin) 
  • Pharmacologically active Toxins (Cholera Toxin) (changes the activity of enzymes) 
  • Neurotoxins (tetanospasmin, C. botulinum Toxin) (the central nervous system is damaged) 
  • Endotoxins
Q:

On what depends virulence?

A:

=ability of the pathogen to cause damage, also factors to help the pathogen with colonizing the host 

Pathogen 

  • Invasion 
  • Toxicity 


Host 

  • General fitness 
  • Health status (chronic or acute diseases)
  • Immune status (chemo-radio patients, HIV) 
  • Extreme stress 
  • Age & gender 
  • Genetic factors
Q:

What does dynamic virulence mean?

A:

Bacteria can evolve from non-pathogens to become pathogens through acquisition of new genetic material. Pathogenic bacteria can undergo further genetic modification that leads to altered virulence and changes in their genome.

Q:

3 Types of re-emerging diseases

A:

1) Evolution of new strains within the same host species (methicillin-res S. aureus MRSA)

2) Switch to new host species (MRSA, HIV, SARS-CoV, covid-19 causing SARS--CoV-2)

3) Switch to new host species plus change in geographic range (West Nile virus in America)

Immunologie B

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