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IMMUNOLOGY (foundation B) > 32. Innate immune system > Flashcards

32. Innate immune system Flashcards

1
Q

CELLULAR MEDIATORS in innate immune system

A

Macrophages
Neutrophils
Dendritic cells
Mast cells

(have Epithelium barrier)

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2
Q

SOLUBLE MEDIATORS / extra-cellular mediators in innate immune system

A

Cytokines
Complement
Acute phase protein
Antimicrobial factors

(have mucus antimicrobial factors barrier)

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3
Q

major INTERFACES between the body and external environment include… (4)

A
  • SKIN
  • GASTROINTESTINAL TRACT
  • RESPIRATORY TRACT
  • GENITOURINARY TRACT
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4
Q

Microbes come into contact with INTERFACES via… (4)

A
  • PHYSICAL CONTACT
  • INGESTION
  • INHALATION
  • SEXUAL ACTIVITY
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5
Q

what forms a MECHANICAL BARRIER against Microbes

A

continuous EPITHELIA

-consisting of TIGHTLY ADHERENT CELLS

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6
Q

SKIN is made of

A

STATIFIED SQUAMOUS EPITHELIUM

(several stacked layers of cells)

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7
Q

How do OUTERMOST LAYERS of SKIN act as a BARRIER against MICROBES

A
  • DRY and INHOSPITABLE to microbes
  • regular sloughing (SHEDDING) helps reduce microbial load
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8
Q

how does SKIN act as a BARRIER to MICROBES (5)

A
  • WATER-RESISTANT (lipids in inner-layer provide additional waterproof barrier)
  • SWEAT: HIGH SALT content and LOW PH INHIBITS BACTERIAL GROWTH
  • contains ANTI-MICROBIAL PROTEINS
  • outermost layer DRY and INHOSPITABLE
  • regular SHEDDING helps reduce microbe loading
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9
Q

keratinocytes in skin produce keratin which protects epithelial cells from..

A

damage, stress

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10
Q

MUCOUS MEMBRANES of EPITHELIAL surfaces consist of…

A

one or more LAYERS of EPITHELIAL CELLS OVERLYING a LOOSE LAYER of CONNECTIVE TISSUE

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11
Q

where are MUCOUS MEMBRANES found (3)

A
  • GASTROINTENSTINAL (GI) TRACT
  • RESPIRATORY TRACT
  • UROGENITAL TRACT
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12
Q

what does MUCUS do in mucous membranes

A

ADHESIVE BARRIER that TRAPS PATHOGENS

  • produced by Goblet cells in epithelium or specialised Submucosal Glands
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13
Q

in RESPIRATORY tract, what happens to PATHOGENS TRAPPED in MUCUS

A

Expelled by movement of CILLIA

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14
Q

How does GI TRACT act as a BARRIER against PATHOGENS

A
  • LOW PH of GASTRIC SECRETIONS
    INHIBIT BACTERIAL GROWTH
  • PERISTALSIS MOVES PATHOGENS
    through GI tract
  • NORMAL FLORA (microbiota) may
    OUTCOMPETE pathogens.
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15
Q

how do NORMAL FLORA of GI TRACT act against PATHOGENS

A
  • COMPETE with pathogens (outcompete)

compete for NUTRIENTS or physical SPACES that would otherwise be occupied by pathogens,
strengthen epithelial barriers,
PRODUCE ANTI-MICROBIAL FACTORS of their own.
- stimulate DEVELOPMENT of the IMMUNE SYSTEM.

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16
Q

EPITHELIAL CELLS secrete soluble mediators that contribute to HOST DEFENCE: (3)

A
  • produce ANTIMICROBIAL substances
  • release CHEMOKINES
    chemotactic signals to RECRUIT IMMUNE CELLS
  • release CYTOKINES
    to COMMUNICATE with IMMUNE CELLS
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17
Q

examples of ANTIMICROBIAL PROTEINS produced by EPITHELIAL CELLS

A

(enzymes)
- Lysozyme
- Secretory
Phospholipase A2

(Antimicrobial Peptides)
- Defensins
- Cathelicidins
- Histatins

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18
Q

besides epithelial cells what also PRODUCE ANTIMICROBIAL PROTEINS

A

PHAGOCYTIC CELLS

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19
Q

STEM cells in the GUT are responsible for…
protected by…

A

the ability of the epithelium to RENEW and REPAIR itself

  • PROTECTED by PANETH CELLS
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20
Q

what are OPSONINS

A

the PROTEINS that decorate the SURFACE of the PATHOGEN

PHAGOCYTES have SPECIFIC RECEPTORS for the OPSONINS,
allowing them to ATTACH to the
pathogen, and ENGULF and DESTROY it

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21
Q

what is OPSONISATION

A

COATING of an infectious agent with HOST PROTEIN which makes
it more easily RECOGNISED by PHAGOCYTES

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22
Q

what are CHEMOKINES

A

FAMILY of CYTOKINES

  • DIRECT the MIGRATION of IMMUNE CELLS (CHEMOTAXIS)
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23
Q

how do CHEMOKINES DIRECT the MIGRATION of IMMUNE CELLS

A

UP a CONCENTRATION GRADIENT

TOWARDS the SOURCE of the chemokine

  • CHEMOTAXIS
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24
Q

The ABILITY of a cell to RESPOND to a particular CHEMOKINE GRADIENT depends on…

A

the EXPRESSION of CHEMOKINE RECEPTORS on the cell surface.

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25
Q

where are ACUTE PHASE PROTEINS produced..

A

LIVER

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26
Q

ACUTE PHASE PROTEINS are produced in response to…

A

INFLAMMATION

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27
Q

release of ACUTE PHASE PROTEINS from liver is stimulated by…

A

CYTOKINES (IL-6) from sentinel cells

(which are activated in response to PAMPS/DAMPS)

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28
Q

FUNCTIONS of ACUTE PHASE PROTEINS: (4)

A
  • RECRUITMENT of immune cells
  • Pattern recognition (bind to bacterial and fungal polysaccharides and
    glycolipids) and activation of COMPLEMENT CASCADE
  • Binding to pathogens and enhancing UPTAKE by PHAGOCYTIC cells =
    OPSONISATION
  • BINDING to, and KILLING pathogens.
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29
Q

what are COLLECTINS

A
  • ACUTE PHASE PROTEINS
  • Molecules that ACT AS Soluble PATTERN RECOGNITION RECEPTORS
  • BIND OLIGOSACCHARIDES or LIPIDS on MICROBIAL SURFACES (PAMPs)
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30
Q

what are EXTRA-CELLULAR INNATE MEDIATORS and their functions

A
  • A wide variety of soluble mediators
  • Some are constitutive, some inducible: e.g. acute phase proteins
  • Bind to pathogens and BLOCK their CELLULAR RECEPTORS
  • Bind to pathogens and KILL them directly
  • Bind to pathogens and ENHANCE their UPTAKE by phagocytic cells
    (opsonisation)
  • RECRUIT immune cells (CHEMOTAXIS)
  • ACTIVATE immune cells and SYSTEMIC INFLAMMATORY RESPONSE
    (cytokines)
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31
Q

what is the COMPLEMENT SYSTEM

A

Family of abundant SERUM PROTEINS

  • involved in DETECTION and DESTRUCTION of pathogens

C1-C9

(can be considered as an extracellular innate mediator)

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32
Q

3 ways the COMPLEMENT SYSTEM can be ACTIVATED

A
  • CLASSICAL
    via ANITBODY
  • ALTERNATIVE
    via direct contact with PATHOGEN
  • LECTIN
    via CARBOHYDRATE BINDING MEDIATORS
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33
Q

each COMPLEMENT PATHWAY starts with…

A

RECOGNITION of the surface of a MICROBE

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34
Q

every COMPLEMENT PATHWAY results in…

A

CLEAVAGE OF C3

into C3b and C3a

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35
Q

what is C3a

A

an ANAPHLATOXIN

increases VASODILATION and VASCULAR PERMEABILITY

plays a role in RECRUITMENT of INNATE immune cells

(smaller)

36
Q

what is C3b

A

OPSONIN

enhances DEGRADATION of pathogens by PHAGOCYTES

37
Q

CLEAVAGE of C3 in complement system relies on the GENERATION of…

A

C3 CONVERTASE

38
Q

in COMPLEMENT activation, the COVALENT BINDING of C3b to other molecules results in the formation of…

A

C5 CONVERTASE

-generates C5a & C5b

39
Q

C5a acts as… (2)

A

ANAPHYLATOXIN &
CHEMOATTRACTANT

40
Q

C5b becomes part of/forms the…

A

MEMBRANE ATTACK COMPLEX
(binds with C6,C7,C8,parts C9)

which results in CELL LYSIS

(make ion channels that allow water movement but not protein)

41
Q

ACTIVATION of COMPLEMENT is referred to as..

A

the COMPLEMENT CASCADE

42
Q

examples of Pathogen-associated Molecular Patterns (PAMPs)

(molecular signatures shared across groups of bacteria, fungi or viruses, but not commonly found on host cells)

A

Flagellin
LPS
Peptidoglycan
ds RNA (viral)
ss RNA (viral)
Unmethylated CpG
DNA (bacterial)

43
Q

examples of Damage (danger)-associated Molecular Patterns
(DAMPs)
(host proteins released from cells or generated from tissues following injury)

A

Extracellular DAMPs:
Hyaluronic Acid
Heparan sulfate
Collagen-derived peptides
Fibrinogen

Intracellular DAMPs:
HMGB1
Uric Acid
Chromatin
Heat-shock proteins
N-formyl peptides

44
Q

what is HMGB1 - High mobility group box 1 protein

A

INTRACELLULAR DAMP

Involved in CHROMATIN REMODELLING and REGULATION of TRANSCRIPTION

Released into extracellular space by NECROTIC cells,
or secreted by immune cells in INFLAMMATION

45
Q

Pattern Recognition Receptor Families:

A
  • TOLL-LIKE receptors (TLR)
  • NOD-LIKE receptors (NLR)
  • C-TYPE LECTIN receptors (CLR)
  • RETANOIC ACID-INDUCIBLE GENE-1 LIKE RECEPTORS (RLR)
46
Q

TOLL-LIKE receptors (TLR)
location?
ligands?
ligand sources?
recognise..

A

PLASMA MEMBRANE (Including vesicular membranes/endosomal membranes)

Ligands: LPS, DNA, RNA, peptidoglycan, flagellin, DAMPs

Ligand Sources: Bacteria, viruses, parasites, self

recognise NUCLEIC ACIDS of ingested microbes

47
Q

NOD-LIKE receptors (NLR)
location?
ligands?
ligand sources?
recognise..

A

CYTOPLASM

LIgands: DAMPs, muramyldipeptides (fragments of
peptidoglycan)
Ligands Source: Self, bacteria

recognise BACTERIAL CELL WALL LIPIDS
and PRODUCTS of DAMAGED HOST CELLS

48
Q

C-TYPE LECTIN receptors (CLR)
location?
ligands?
ligand sources?
recognise..

A

PLASMA MEMBRANE

Ligands: Beta-glucans

Ligands Source: Fungi

recognise MICROBIAL POLYSACCHARIDE

49
Q

RETANOIC ACID-INDUCIBLE GENE-1 LIKE RECEPTORS (RLR)
location?
ligands?
ligand sources?
recognise..

A

CYTOPLASM

Ligands: double-stranded RNA viruses

Ligand Source: RNA viruses

recognise VIRAL RNA

50
Q

TOLL-LIKE RECEPTOR family has how many members…

A

9

51
Q

TOLL-LIKE RECEPTORS are specific to either…

A

GRAM-POSITIVE BACTERIA

GRAM-NEAGATIVE BACTERIA
(TLR-1, TLR-4)

or viruses (3,7,8)

52
Q

where are TLR-1, TLR-2, TLR-3, TLR-4, TLR-5, TLR-6 found

A

CELL SURFACE

53
Q

where are TLR-3, TLR-7, TLR-8,TLR-9 found

A

ENDOSOME

54
Q

why do we have so many different PRRs

A
  • We are up against a vast range of different bacterial, viral and fungal pathogens with a great VARIETY of antigenic EPITOPES
  • Many pathogens can AVOID RECOGNITION by the host immune response hence we need several BACKUP MECHANISMS should one or more be evaded
55
Q

DENDRITIC CELLS express which TLR

A

TLR-4

56
Q

what happens when TLR-4 is ACTIVATED on DENDRITIC CELLS
- to enhance ADAPTIVE immune response
(by PAMPs/DAMPs)

A
  • Induces production of PROINFLAMMATORY CYTOKINES
  • Induces UPREGULATION of costimulatory molecules
    CD80/CD86 required for T-CELL ACTIVATION
  • Leads to UPREGULATION of CLASS II MHC
57
Q

Recruitment of neutrophils to the site of infection:
At the site of infection, cells that have encountered microbes can produce…

A

CYTOKINES eg. TNF alpha, Interleukin-1

58
Q

Recruitment of neutrophils to the site of infection:
Cytokines produced by cells at site of infection ACTIVATE ENDOTHELIAL CELLS to EXPRESS…

A
  • SELECTINS
  • INTEGRIN RECEPTORS
  • SECRETE CHEMOKINES
59
Q

Recruitment of neutrophils to the site of infection:
SELECTINS, INTEGRIN LIGANDS and CHEMOKINES produced by endothelial cells causes…

A
  • selectins activate: ROLLING of neutrophils from blood
  • integrins activate: stable ADHESION of neutrophils to venule (integrin activation by chemokines)
  • chemokines activate: neutrophil MIGRATION THROUGH ENDOTHELIUM to site of infection
60
Q

what is the result of Recruitment of neutrophils to the site of infection

A

PHAGOCYTOSIS and destruction of pathogen

activated when cell surface receptors bind to opsonins of the pathogen

61
Q

when PHAGOSOME releases its contents in the PHAGOLYSOSOME what happens

A

OXIDATIVE BURST
- generating oxidative species

62
Q

what does the PHAGOSOME FUSE with

A
  • NEUTROPHIL GRANULES
  • LYSOSOMES

phagolysosome

63
Q

what leads to pathogen destruction in phagosome

A

combined activities of REACTIVE OXYGEN SPECIES and GRANULE CONTENTS (nuclear proteases)

64
Q

6 steps of PHAGOCYTOSIS

A
  1. Phagocytosis is initiated when CELL SURFACE RECEPTORS BIND to components of the PATHOGEN surface, or OPSONINS (e.g. antibodies, complement proteins).
  2. The pathogen is engulfed: SURROUNDED BY PLASMA MEMBRANE , and
    internalised into a LARGE VESICLE (PHAGOSOME)
  3. The phagosome FUSES with NEUTROPHIL GRANULES and
    LYSOSOMES. The CONTENTS are DISCHARGED into the PHAGOSOME.
  4. An OXIDATIVE BURST is initiated in the phagosome, generating
    REACTIVE OXYGEN SPECIES (ROS)
  5. Combined activities of REACTIVE OXYGEN SPECIES and GRANULE CONTENTS (neutral proteases) lead to pathogen DESTRUCTION
  6. EXOCYTOSIS of SOLUBLE DEBRIS
65
Q

NEUTROPHIL PRODUCTS and their EFFECTS

A

GELATINASE - Degradation of host tissue

LACTOFERRIN - Binds to IRON (competes with pathogens for iron so limited availability for pathogens)

ELASTASE - Degradation of host tissue/microbes

COLLAGENASE - Degradation of host tissues

MYELOPEROXIDASE - Respiratory Burst

LYSOZYME - Kills Bacteria

DEFENSINS - Kills Bacteria

Bacterial Permeability Inducing Factor - Kills Bacteria

66
Q

NEUTROPHILS also undergo…

A

NETOSIS

67
Q

for NETosis NEUTROPHILS release…

A

NEUTROPHIL EXTRACELLULAR TRAPS (NETs)
- web of fibres composed of chromatin and anti-microbial factors

68
Q

what do NETs do in NETosis of NEUTROPHILS

A

TRAP and KILL extracellular MICROBES

69
Q

what are required for the formation of NETs in NETosis

A

reactive oxygen species (ROS)

activation of PROTEASES

70
Q

first line of defence cells:

A

neutrophils

71
Q

INNATE LYMPHOID CELLS are considered to be the INNATE COUNTERPARTS (equivalents) of…

A

T CELLS

( do NOT express T cell receptors TCRS)

72
Q

INNATE LYMPHOID CELLS are … resident

A

TISSUE RESIDENT

73
Q

INNATE LYMPHOID CELLS stimulated by

A

CYTOKINES at site of infection / damaged epithelia

74
Q

INNATE LYMPHOID CELLS RAPIDLY secrete..

A

CYTOKINES

75
Q

5 subsets of INNATE LYMPHOID CELLS :

A

ILC1
ILC2
ILC3
NK CELLS (natural killer)
Lti CELLS

76
Q

INNATE LYMPHOID CELLS are involved in…

A

the protective immune response to pathogenic
microbes
/ tissue homeostasis and tissue repair.

ILC DYSFUNCTION is thought to play a role in asthma, autoimmune disease

77
Q

NATURAL KILLER (NK) CELLS are …. derived LYMPHOCYTES

A

BONE-MARROW DERIVED lymphcytes

making up around 10% of peripheral lymphocytes

78
Q

NK cells are bone-marrow derived LYMPHOCYTES lacking…

A

antigen-specific receptors of T or B cells

79
Q

NK CELLS are important in PROTECTION against..

A

VIRAL INFECTION or CANCEROUS CELLS

RECOGNISE and KILL STRESSED cells / INFECTED cells
- release GRANULES that kill target cell

specialised NK cells found in placenta play an important role in pregnancy

80
Q

NK cells respond to which CYTOKINE

A

IL-12 (interleukin-12)
- stimulates release of Interferon Gamma
- activates macrophage to kill microbe

81
Q

NK CELLS express both receptors:

A

ACTIVATING RECEPTOR
& INHIBITORY RECEPTOR

82
Q

NK CELLS:
what do HEALTHY HOST CELLS express..

A

CLASS I MHC MOLECULES

83
Q

NK CELLS:
CLASS I MHC molecules on HEALTHY HOST CELL is recognised by…

A

INHIBITORY RECEPTOR of NK CELLS

  • inhibitory receptor not engaged
84
Q

how do we get ACTIVATION of NK CELLS

A

NO MHC CLASS I on the cell
( not healthy cell - virus inhibits CLASS I expression)
so INHIBITORY RECEPTOR NOT ENGAGED

only ACTIVATING RECEPTOR is ENGAGED

85
Q

recognitional of microbial components by PRR leads to..

A

MATURATION of DENDRITIC CELLS

  • activates ADAPTIVE immune system

IMMUNOLOGY (foundation B) (7 decks)

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