Immunology: Review of The Innate Immune System Flashcards

1
Q

Why do we need both innate and adaptive immunity to protect us from infection?

A
  • We need innate immuntity as it provides immediate and early protection against pathogens
  • We need adaptive immunity as it provides ‘memory’ of an infection which makes it easier to recover next time we’re infected by the same/similar pathogen
  • Innate immunity may not be enought to protect us from certain pathogens so adaptive immuntiy also needed
  • Adaptive Immunity is too slow to protect us from some new pathogens
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2
Q

What’s the difference in specificity betwen innate and adaptive immunity?

A
  • Adaptive immunity – Involves very specific recognition of infectious agent (usually sees an antigen on surface of pathogen)
  • Innate immunity - Doesn’t involve specific antigen recognition but does involve recognition of broadly conserved features of different classes of pathogens
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3
Q

What are the components of innate immunity?

A
  • Phagocytosis
  • The Inflammatory Response
  • Cytokines, Interferons and Antimicrobial peptides (AMPs)
  • Complement
  • Intrinsic Defences – “the hostile cell”
  • Natural killer (NK) cells
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4
Q

What immune system cells carry out phagocytosis?

A
  • Dendritic cells
  • Macrophages
  • Neutrophils
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5
Q

What role do dendritic cells have in innate immunity?

A
  • Detect a pathogen, take it up and then stop any further phagocytosis
  • They then move to lymph nodes where they break down the pathogen they’ve taken up
  • They then present the pathogens peptides on its surface via MHC class II/I presentation which stimulates adaptive immune response
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6
Q

What roles do machrophages have in innate immunity?

A
  • Phagocytosis - material is destroyed in lysosomes
  • Captured material can trigger macrophage activation - activated macrophages produce cytokines and chemokines to stimulate both innate and adaptive immune responses
    • This triggers the inflammatory response and can promote a local anti-microbial state
  • Involved in clearing and repairing damage
  • NOTE: Most of them are tissue resident
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7
Q

What roles do neutrophils have in innate immunity?

A
  • Rarely tissue resident - they’re circulating within bloodstream
  • When there’s an infection they get recruited to site of infection/inflammation
  • They carry out most of the phagocytosis
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8
Q

What is the inflammatory response?

A
  • A generic defence mechanism whose purpose is to localize and eliminate injurious agents and to remove damaged tissue components
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9
Q

What things does the inflammatory response cause?

A
  • Localised infection - stops pathogens frm leaving site of infection
  • Removes pathogen via phagocytosis
  • Repairs tissue damage from previous infection
  • Enhances permeability of endothelium and extravasation
  • Neutrophil recruitment
  • Enhances cell adhesion - Makes cells sticky which prevents neutrophils from leaving
  • Enhances clotting - Creates physical environment which makes it harder for pathogens to spread
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10
Q

What are cytokines?

A
  • Glycoprotein hormones that affect the immune response
  • Act as a very specific signal of a component of the immune response
    • Have a very defined narrow role that helps immune system
  • Act to modify the behaviour of cells in the immune response
  • Most of these are called interleukins (eg. IL-1), some called interferons and TNF
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11
Q

What are chemokines?

A
  • Glycoprotein hormones that affect the immune response
  • Secreted at site of infection like chemokines
  • Act as chemotactic factors – they create concentration gradients which attract (or occasionally repel) specific cell types to a site of production/infection
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12
Q

How do phagocytes know what targets to phagocytose?

A
  • By detecting phosphatidylserine on exterior membrane surface - Indicates cells undergoing apoptosis as phosphatidylserine located on inside of healthy cell
  • By Scavenger receptors -
  • By some Toll-Like Receptors (TLRs) - Play very little role in recogniation of material to be phagocytosed
  • By passive sampling - At site of infection cells phagocytose things at random (mainly done by neutraphils)
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13
Q

What are PAMPs?

A
  • PAMPs = Pathogen-associated Molecular Patterns
  • Molecules present only on pathogens and not on host cells
  • Essential for survival of pathogens
  • Invariant structures (can’t be changed) tahte are shared by entire class of pathogens
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14
Q

What are some examples of PAMPs?

A
  • Gram-negative bacteria - All have lipopolysaccharides (LPSs) found in outer membrane
  • Gram-positive bacteria - All have teichoic acid, lipoteichoic acid and peptidoglycan found in outer membrane
  • Bacterial flagella
  • Abnormal protein glycosylation
  • Abnormal nucleic acids - viral nucleic acid slightly different to host cell nucleic acid
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15
Q

What are pattern recognition receptors (PRRs)?

A
  • Host factors that specifically recognise a particular type of PAMP
  • They are germ-line encoded - always express the exact same thing in whatever cell they are expressed in
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16
Q

What are the 3 main functional classes of pattern recognition receptor?

A
  • Extracellular - They recognise PAMPs outside of a cell and trigger a co-ordinated response to the pathogen
  • Intracellular (cytoplasmic) - They recognise PAMPs inside a cell and act to co-ordinate a response to the pathogen
  • Secreted - They act to tag circulating pathogens for elimination
17
Q

What are some examples of pattern recognition receptors?

A
  • Lectin receptors
  • Scavneger receptors
  • Toll-like receptors
  • NOD-like receptors
  • RIG-like receptors (RIG-1 and MDA5)
18
Q

What was the complement system originally described as?

A
  • Originally described as a heat-sensitive component of serum that could augment the ability of antibodies to inactivate antigens
19
Q

What was the complement system originally thought to lead to?

A
  • Thought to be a biochemically complex antibody-dependent effector mechanism leading to:
    • Opsonisation - Complement gets recruited and forms shell of complement protein around pathogen
    • Recruitment of phagocytic cells
    • Vasoactive function - Releases peptides which increase permeability of endothelium
    • Punching of holes in target membranes - Ocurs via membrane attack system (MAC)
20
Q

What do we now know about the complement system?

A
  • Ancient system which predates the development of the adaptive immune response
  • Its use as an effector mechanism for the adaptive immune response is an adpation that was grafted onto its original purpose as a vital part of innate immunity
21
Q

What do complement proteins act as?

A
  • Act as secreted Pattern recognition receptors (PRRs) and can be activated by a range of PAMPs, as well as by “altered self”
22
Q

What are interferons and how do they work?

A
  • Secreted Glycoprotein factors (type I and type III)
  • Induced by viral infection - Major part of anti-viral immune response
  • Produced during primary infection
  • Interferon binds to neighbouring cells that have the receptor for it
  • Triggers antiviral state in neighbouring cells
23
Q

Describe how the interferon system works?

A
  • Cell infected by a virus
  • No immune response against virus in primary infected cell so it’ll apoptose and die
  • Primary infected cell also releases lots of new viral particles which attempt to infect neighbouring cells
  • However, this doesn’t occur
  • This is because interferon produced during primary infection
  • It binds to its receptor on neighbouring cells which triggers anti-viral state in those cells
    • Does this by promoting Transcriptional activation of >400 antiviral response genes
  • This prevents new viral particles from infecting neighbouring cells
24
Q

What are some of the effects of the activation of the various anti-viral response genes in a cell via interferon?

A
  • Cell growth arrest
  • Cell death
  • mRNA degradation
  • Translational arrest
25
Q

What are anti-microbial peptides and how do they work?

A
  • Anti-microbial peptides (AMPs) are secreted short peptides (18-45 amino acids)
  • Usually work by inserting into cell wall and assembling into pores
  • This causes disruption of cell wall leading to lysis
  • Some are induced by bacterial infection
  • Example: Defensins
26
Q

Explain the concept of the “hostile cell”

A
  • Cells themselves have biochemical mechanisms that prevent viral replication
  • Examples of these biochemical mechanisms include:
    • Apoptosis
    • Restriction factors/Intrinsic Immunity
    • Epigenetic silencing
    • RNA silencing
    • Autophagy/Xenophagy - removal of unnecessary or disfunctional components/
27
Q

What are natural killer (NK) cells and what is there structure?

A
  • Large granular lymphocytes - Lymphocyte-like, but larger with a granular cytoplasm
  • Make up 4% of white blood cells
  • Kill certain tumour cells and virally-infected cells via cytotoxic molecules called granzymes & perforins
28
Q

How are natural killer cells activated?

A
  • NK cells possess the ability to recognise and lyse virally infected cells and certain tumour cells
  • Selectivity is conferred by LOSS of “self” MHC molecules on target cell surfaces, and up-regulation of activating ligands
  • Uninfected cell
  • Normally an uninfected cell would present a peptide to NK cell via MHC class I
  • NK Cell recognises peptide presented by MHC Class I
  • This acts as inhibitory signal so NK cells won’t kill the uninfected cell
  • Infected cell
  • Pathogen down-regulates production of MHC Class I resulting in loss of MHC class I on infected cell
  • NK cells able to recognise absence of MHC class I (no inhibitory signal)
  • This causes NK cell to kill infected cell
29
Q

Comaprae and contrast the cell types, speed, memory, specificity, receptors and strategy of recognition between innate and adaptive immunity

A