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Microbiology and Immunology > Review of Innate System > Flashcards

Review of Innate System Flashcards

1
Q

Why do we need an innate immune response when a adaptive immune response is present?

A

Adaptive response is too slow to protect against new pathogens (new microbe replication fast and peaks quickly and adaptive immune system only comes after this peak) - for survival until adaptive immune response comes in

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2
Q

How specific is adaptive immunity?

A

Very specific recognition of infectious agent through protein/antigen

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3
Q

How specific is innate immunuty?

A

No specific antigen recognition

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4
Q

What part of pathogens are recognised by innate immunity

A
  • recognises broadly conserved feautures on pathogens - PAMPs (pathogen associated molecular patterns)
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5
Q

What are PAMPs? + what is their purpose

A

Molecules present only on pathogens not on host cells so recognised as non self - found on all pathogens (diff types) - needed for pathogen survival

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6
Q

What type of bacteria are PAMPs found on?

A

gram positive and negative

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7
Q

What is the PAMP on gram negative bacteria?

A

lipopolysaccharides found in outer membrane

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8
Q

What is the PAMP on gram positive bacteria?

A

TETICHOIC ACID, peptidoglycan, lipoteichoic acid in outer membrane

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9
Q

Give examples of general PAMPs? in diff types of pathogen

A

Bacterial flagella
Abnormal protein glycosylation
Abnormal nucleic acids - viruses

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10
Q

What part of host recongises PAMPs?

A

PRR (pattern recognition receptor)

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11
Q

Why are viruses PAMPs nucleic acid?

A

Dont have cell wall to recongise things on surface of the pathogen

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12
Q

What does germ line encoded mean? + example of something that is germ line encoded

A

receptors that Cannot be rearranged somatically - PRRs

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13
Q

What are the classes of PRRs? and what does each do

A

Intracellular - (cytoplasmic) recognise PAMPs inside a cell - pathogen has already entered cell
Extracellular - recognise PAMPs outside cell - before pathogen enters cell
Secreted - tag circulating pathogens for elimination

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14
Q

How can you experiment mice reaction to see what would happen if they dont have innate response

A

Get rid of PRRs so no receptors to recognise PAMPs (general recongition in innate immunirt)

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15
Q

What are all the component of innate immunity?

A 
Inflammatory response
Phagocytes
Complement
Cytokines, chemokines, and anti-microbial peptides (AMPs)
Natural killer cells
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16
Q

Name a few phagocytes?

A

Monocytes, NEUTROPHILS, dendritic cells

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17
Q

What is the purpose of an inflammatory response?

A

Generic defense mechanism to localise and eliminate injurious agents/damaged tissue components + prevent pathogen from leaving site of infection

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18
Q

What triggers inflammatory responses?

A

Pro-inflammatory cytokines and chemokines at the site of infeciton

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19
Q

What are the other effects of an inflammatory response?

A

Enhanced permeability and extravasation
Neutrophil recruitment
Enhanced cell adhesion
Enhance clotting

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20
Q

What is extravasation?

A

Cells can pass from blood to tissues

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21
Q

Why is it good to enhance cell adhesion in inflammatory response?

A

Neutrophils and macrophages stick to tissue at site of infection

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22
Q

Why is increased clotting important in inflammatory response?

A

Identifying restriction and restrict - cut off blood supply

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23
Q

Which components of innate immunity is linked to eachother?

A

Phagocytes, complement and cytokines, chemokines + AMPs

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24
Q

What is important about cell recongition in phagocytosis?

A

Need to know which cells are infected to produce correct cytokines and chemokines and not destroy healthy cells

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25
Q

What receptors are on phagocytes and what are their purposes? !!!!!!!!!!!!!

A

Pattern recognition receptors - Toll like receptors involved in making cytokines and chemokines NOT IN the phagocyte recognising pathogen
Diff PRR recognises what to eat and what not to

26
Q

What organisms does phagocytosis happen in?

A

In all multicellular organisms so they all have to recongise and phagocytose debris.infected cells

27
Q

What is different about neutrophils compared to the other phagocytes (macrophages and dendritic cells)?

A

Not involved in priming adaptive immune response , more involved in tissue repair and tissue damage (eating damage at site of infection)

recruited through cytokines produced by macrophages

28
Q

What are the 3 roles of macrophages and dendritic cells ?

A
  • Phagocytosis
  • Macrophages once activated produces cytokines and chemokines to stimulate both innate and adaptive response (triggering inflammatory process)
  • Pathogen peptides broken down and presented through MHC + promotes development/recall of adaptive T cell response
29
Q

How do phagocytes know what to eat?

A

Passive sampling to detect:

  • atypical sugars (mannose or beta glucan) or phosphatidlyserine (on outside of surface for apoptosing cells)
  • complement proteins bound on pathogen surface
30
Q

What phagocytic receptors are present on macrophages (to recongise what to eat)?

A 
Complement receptors
Mannose reeptors
Lipid receptors
Scavenger receptors (NOT TOLL LIKE RECEPTORS)
beta glucan receptor
31
Q

Why might cells be already going under apoptosis that phagocytes need to recongise?

A

Many viruses cause apoptosis, if phagocytes recognise these by recognising phosphatidylserine out outer surface, macrophages can ingest those cells

32
Q

What do scavenger receptors recognise?

A

Non self particles on surface of our cells

33
Q

What is passive samping?

A

Phagocytes constantly drinking up debris from environment

34
Q

What is the complement system?

A

Heat sensitive component of serum that increase ability of antibodies to inactivate antigen and complement proteins act as PRR that can be activated by PAMPs (increase phagocytosis

35
Q

What are the 3 pathways in the complement system?

A

Classical pathway
Lectin pathway
Alternative pathway

36
Q

What activates the classical pathway of complement?

A 
Antigens (PAMP) recongised by antibodies (PRR)
\:ipopoylsaccharides (PAMP) recongised by lipoprotein (PRR)
Abnormal phospholipids (PAMP) recongised by pentraxins (PRR)
37
Q

What is the lectin pathway?

A

Complement system

The pamps recognised are atypical glycosylation

38
Q

What is the alternative pathway?

A

Lack of control factors (cells have complement control factors so complement does not attack host cells, lack of means cell is seen as non self and activates alternative pathway)

39
Q

Which PRR receptors involved in phagocytes knowing when cells are infected and when to produce chemokines and cytokines? (not the receptors that tell phagocytes what to eat and what not to eat)

A

Toll like receptors
NOD-like receptors
RIG-like receptors

43
Q

What are cytokines? example

A

GLYCOPROTEIN HORMONES that modify behaviour of cells in immune response

most are interleukins

44
Q

What are chemokines?

A

GLYCOPROTEIN HORMONES that act as chemotactic factors( create concentration gradient to attract specific cells types to site of infection)

45
Q

What are interferons?

A

Main anti-viral cytokines (secreted glycoprotein hormone induced by viral infection)

46
Q

What types of cytokines are interferons?

A

Type 1 (protect other surfaces in blood stream and tissues) and type 3 (protect epithelial cells e.g. lungs)

47
Q

Why are interferons useful?

A

No they provide CROSS-PROTECTION (interferons produced for one infection can protect from another viral infection e.g. interferons produce from flu can protect against polio

48
Q

Describe the process of interferons providing protection step by step?

A

Interferon made by primary infected cell that dies
Released Interferon binds to neighbouring cells triggering transcription of antiviral genes so cell doesnt allow replication when virus tries to spread - cell is now in an ANTI-VIRAL STATE (cell wont be permissive of the virus being let in or replicating)

49
Q

What is the signal pathway once interferon binds to a neighbouring cell receptor?

A

Signal transduction e.g. JAK-STAT pathway

e.g protein kinase made causing translational arrest of viral rna and cellular rna will also not be translated but also prevents rna from virus replicating

50
Q

What are AMPs? + example

A

Antimicrobial peptides - short peptides e.g defensins

51
Q

What do AMPs do?

A

Disrupt cell wall leading to lysis. Offer broad protection

52
Q

What are AMPs induced by?

A

Bacterial infection

53
Q

What are NK cells?

A

natural killer cell - large GRANULAR lymphocytes

54
Q

What do NK cells do?

A

Destroy (by lysing) target cells (infected and certain tumour cells) using cytotoxic molecules called GRANZYMES AND PERFORINS

55
Q

What activates NK cells?

A

Loss of self MHC molecules on target cell surfaces AND up regulation of activation ligands (death receptors)

56
Q

What ends up happening if innate immunity is defected?

A

Diseases associated to defect e.g. complement defect = development of autoimmune diseases such as lupus

57
Q

2nd to last slide still needs flashcards

58
Q

Compare speed in innate vs adaptive immunity?

A

Innate is fast, adaptive is slow

59
Q

Compare memory in innate vs adaptive immunity?

A

No memory in innate, yes in adaptive

60
Q

Compare receptors in innate vs adaptive immunity?

A

PRRs in innate

Ig and TCR in adaptive

Microbiology and Immunology (31 decks)

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