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π’»π“Šπ“ƒπ’Ήπ’Άπ“‚π‘’π“ƒπ“‰π’Άπ“π“ˆ π‘œπ’» π“…π’Άπ“‰π’½π‘œπ“π‘œπ‘”π“Ž > Innate immunity > Flashcards

Innate immunity Flashcards

1
Q

what are the sites of microbe entry?

A 
β†’Conjunctiva 
β†’Arthropod 
β†’Capillary 
β†’Scratch
β†’ injury 
β†’Skin 
β†’Anus 
β†’Urinogenital tract 
β†’Alimentary tract 
β†’Respiratory Tract
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2
Q

describe the inflammatory response

A

β†’ generic defence mechanism
β†’to localize and eliminate injurious agents
β†’remove damaged tissue components
β†’enhanced permeability and extravasation

β†’ Neutrophil recruitment
β†’ Enhanced cell adhesion
β†’Enhance clotting
β†’Triggered by the release of pro-inflammatory cytokines and chemokines at the site of infection

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3
Q

what do cytokines do?

A

β†’Act to modify the behaviour of cells in the immune response
β†’Most of these are called interleukins (eg. IL-1

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4
Q

what do chemokines do?

A

β†’Act as chemotactic factors
β†’ i.e. they create concentration gradients which attract (or occasionally repel) specific cell types to a site of production/infection

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5
Q

what is IL-1?

A

β†’Main producer = Macrophages + keratinocytes
β†’Acts upon = lymphocytes + liver
β†’Effect = Enhances response
β†’ Induces acute-phase protein secretion

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6
Q

what is IL-6?

A

β†’ Main producer = Macrophages + dendritic cells
β†’ Acts upon = lymphocytes + liver
β†’ Effect = Enhances response
β†’ Induces acute-phase protein secretion

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7
Q

what is CXCL8 (IL-8)?

A

β†’Main producer: Macrophages + dendritic cells
β†’Acts upon: Phagocytes
β†’Effect: Chemoattractant for neutrophils

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8
Q

what is IL-12?

A

β†’Main producer: Macrophages + dendritic cells
β†’ Acts upon: Naive T cells
β†’Effect: Diverts immune response to type 1, β†’proinflammatory, cytokine secretion

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9
Q

what is TNF - alpha?

A

β†’Main producer: Macrophages + dendritic cells
β†’Acts upon: Vascular endothelium
β†’Effect: Induces changes in vascular endothelium (expression of cell-adhesion molecules (E- + P- selectin), changes in cell-cell junctions w/increased fluid loss

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10
Q

how do macrophages β€œsee” microbes?

A

β†’Passive sampling
β†’ Scavenger receptors
β†’Engulfing apoptotic cells

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11
Q

what are examples of Pathogen-associated Molecular Patterns (PAMPs)?

A

β†’Gram-negative bacteria; lipopolysaccharides (LPSs) found in outer membrane

β†’Gram-positive bacteria; teichoic acid, lipoteichoic acid, peptidoglycan found in outer membrane

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12
Q

what are other PAMPs?

A

β†’Bacterial flagellin
β†’Abnormal protein glycosylation
β†’Abnormal nucleic acids - viruses

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13
Q

what are Pattern recognition receptors (PRRs)?

A

β†’Host factors that specifically recognise a particular type of PAMP
β†’They are germ-line encoded

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14
Q

what are the three classes of PRRs?

A

Extracellular
β†’ they recognise PAMPs outside of a cell and trigger a co-ordinated response to the pathogen

Intracellular (cytoplasmic)
β†’ they recognise PAMPs inside a cell and act to co-ordinate a response to the pathogen

Secreted
β†’ they act to tag circulating pathogens for elimination

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15
Q

Lectin receptors

A

β†’Ligand: terminal mannose and fucose

β†’Outcome: phagocytosis

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16
Q

Scavenger receptors

A

β†’Ligand: bacterial cell walls modified low-density lipoproteins
β†’Outcome: phagocytosis

17
Q

Toll-like receptors (TLRs) (surface and endosomal)

A

β†’Ligand: LPS (together with CD14) lipoproteins unmethylated CpG flagellin ds RNA; ss RNA (in endosomes)

β†’Outcome: inflammation: cytokine release (TNF, IL-1, IL-12) enhanced killing: reactive oxygen species, NO)

18
Q

NOD-like receptors (NLRs) (cytoplasm)

A

β†’Ligand: peptidoglycan from Gram positive and negative bacteria some viral DNA and RNA (indirect?)

β†’Outcome: inflammation: cytokine release (IL-1, IL-8)

19
Q

RIG-like receptors (RIG-1 and MDA5) (cytoplasmic)

A

β†’Ligand: dsRNA and 5’-triphospho RNA

β†’Outcome: type I interferon production

20
Q

how do macrophages β€œsee” microbes?

A

β†’Passive sampling
β†’ Scavenger receptors
β†’Engulfing apoptotic cells

21
Q

what is the complement and what does it do?

A

β†’system of secreted proteins made in the liver that recognise PAMPs on the surface of microbes and β€œdecorate” or β€œtag” them.

β†’The microbes are then cleared by phagocytosis, β€œopsonised” or they have holes punched in them

22
Q

what are the three ways of activating complement?

A

β†’Recognition of LPS and other PAMPs by the C1q component of β€œclassical” pathway (

β†’Non-host glycosylation is recognised by MBP and other lectins to activate the β€œlectin” pathway

β†’ Membranes that are recognised as β€œnon-self” activate the β€œalternative” pathway

β†’Complement activation involves a proteolytic cascade

23
Q

Natural Killer (NK) cells (Large granular lymphocytes)

A

β†’4% white blood cells
β†’Lymphocyte-like but larger with granular cytoplasm
β†’Kill certain tumour & virally infected cells
β†’ Target cell destruction is caused by cytotoxic molecules called granzymes & perforins

24
Q

how are NK cells activated?

A

β†’NK cells possess the ability to recognise and lyse virally infected cells and certain tumour cells.
β†’Selectivity is conferred by LOSS of β€œself” MHC molecules on target cell surfaces, AND up-regulation of activating ligands

25
Q

how does cell death happen?

A

β†’Perforin + cytotoxic granules

β†’Engagement of death receptors

26
Q

CMV has four gene products which

A

β†’reduce the expression of Class 1 MHC molecules and two class I MHC homologues (UL18 & M144), that give a negative signal to NK cells

27
Q

NK cells bind

A

β†’cells bind HLA-E which carries in its groove a peptide from the leader sequence of classical class I MHC molecules

28
Q

inherited defects associated with Innate Immunity

A

β†’Complement – core defects (e.g. C3) linked to development of autoimmune diseases such as lupus

β†’Complement – non-core defects linked to suspectibility to specific types of pathogens such as Neisseria

Macrophage deficiencies
β†’Chronic granulomatous disease (CGD); No oxidative burst for bacterial killing

Macrophage deficiencies
β†’IRF8 mutations linked to susceptibility to TB Aicardi–GoutiΓ¨res syndrome associated with constitutive production of inflammatory cytokines

Lack of interferon-responsiveness
β†’ sensitivity to viral infection (e.g. measles)

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