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Block 4 ALS > Innate immunity and the inflammatory process > Flashcards

Innate immunity and the inflammatory process Flashcards

1
Q

Timeline of innate imminology (immediate 0-4)

A

infection
recognition by perfomed, non specific effectiors
removal of infectious agent

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2
Q

Early induced response (early 4-96)

A

infection
recognition of microbial -associated molecular patterns
Inflammation recruitment and activation of effector cells
removal of infectious agent

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3
Q

Adaptive immune response (late>96 hours)

A 
Infection
Transport of antigen to lymphoid organs 
Recognition by naive B and T cells
Clonal expansion and differentiation to effector cells
Removal of infectious agent
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4
Q

Non-immunological barriers to infection Skin
Mechanical
Chemical
Microbiological

A

Mechanical
Epithelial cells joined by tight junctions
Longitudinal flow of air or fluid

Chemical
Fatty acids
Antibacterial Peptides

Microbiological
Normal Flora

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5
Q

Non-immunological barriers to infection Gut
Mechanical
Chemical
Microbiological

A

Mechanical
Epithelial cells joined by tight junctions
Longitudinal flow of air or fluid

Chemical
Low pH
Enzymes (pepsin)
Antibacterial Peptides

Microbiological
Normal Flora

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6
Q

Non-immunological barriers to infection lungs
Mechanical
Chemical

A

Mechanical
Epithelial cells joined by tight junctions
Movement of mucus by cilia

Chemical
Antibacterial Peptides

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7
Q

Non-immunological barriers to infection eyes/nose
Mechanical
Chemical

A

Mechanical
Epithelial cells joined by tight junctions
Chemical
Salivary enzymes and lysozymes

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8
Q

describe the classical pathway

A

Antigen antibody complexes (pathogen surfaces)
C1q C1r C1s C4 C2
C3 convertase
C3a C5a
Peptide mediators of inflammation, phagocyte recruitment

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9
Q

describe the MB-Lectin pathway

A

Mannose-binding lectin binds mannose on pathogen surfaces
MBL MASP-1 MASP2 C4 C2
C3 convertase
C3b
Binds to complement receptors on phagocytes
Opsonization of pathogens
Removal of immune complexes

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10
Q

describe the alternative pathway

A

Pathogen surfaces
C3 B D
C3 convertase
C3b
Terminal complement components C5b C6 C7 C8 C9
Membrane-attack complex, lysis of certain pathogens and cells

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11
Q

describe the membrane attack complex

A

C5b binds to C6 and C7
C5b67 complex binds to membrance via C7
C8 binds to the complex and inserts into the cell membrane
C9 molecules bind to the complex and polymerize
1-16 molecules of C9 bind to form a pore in the membrane

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12
Q

desribe the recognition mechaisms of innate immunity

A

Rapid response aka hours
Fixed
Limitted no. of specialities
Constant druing response

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13
Q

desribe the recognition mechaisms of adaptive immunity

A

slow response so weeks and days
variable
numerous highly selective speciatlies
improve during response

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14
Q

tow constants between adaptive and innate immunity

A

common effector mechanisms for the destruction of pathogens

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15
Q

Innate immunity receptor characteristics

A

specificity inherited in the genome
expressed by all cells of a particular type eg macropgages
triggers immediate response
recognizes broad classes of pathogen
interacts with a range of molecular structures of a given type

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16
Q

adaptive immunity receptor characteristic

A

encoded in multiple gene segments
requires gene rearrangement
clonal distribution
able to discriminate between even closely related molecular structures

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17
Q

what initiates the release of cytokines and small lipids mediators of inflammation

A

bacteria binding to macrophage receptors

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18
Q

what does the macrophage have on its surface

A

receptors for many bacterial constituents

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19
Q

how do Pattern recoginition receptors PPR identifies the class of pathogen ?

A

by

recognising “pathogen associated molecular patterns” (PAMPs)

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20
Q

principles of phagocytosis

A 
attachment by pattern recognition receptors 
pseudopodia forming a phagosome
granule fusion and killing
release of microbial
granule fusion and killing
the release of microbial products
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21
Q

during phagocytosis what do phagocytes switch on

A

potent antimicrobial

mechanisms

22
Q

when does the activation of NADPH oxidase happen and what is released

A

during the “Respiratory burst” and
releases toxic oxygen radicals
(superoxide and hydrogen peroxide)

23
Q

what is wrong with the Oxygen radicals

A

may directly damage
microbial membranes and / or activate
microbicidal enzymes found in granules

24
Q

role of phagosomes in innate immunity

A

pathogen killing
pathogen processing
pathogen presentation TLRS
Pathogen presentation to cytosolic sensors NODs/NALPs

25
Q

role of phagosomes in adaptive immunity

A

antigen dgredation
antigen processing
antigen presentation MHCII
Antigen presentation via cytosol MHCI

26
Q

what are the Microbicidal mechanisms of phagocytes and the products

A 
Acidification
Toxic oxygen derived products
Toxic nitrogen oxides
Antimicrobial peptides
Enzymes
Competitors
27
Q

what proportion of leukocytes are Neutrophil

A

40-75

28
Q

what proportion of leukocytes are Eosinophil

A

1-6

29
Q

what proportion of leukocytes are Basophil

A

<1%

30
Q

what proportion of leukocytes are Monocyte

A

2-10

31
Q

what proportion of leukocytes are Lymphocyte

A

20-50

32
Q

what proportion of leukocytes are Dendritic cells

A

<1%

33
Q

how do activated neutrophils catch bacteria

A

“neutrophil extracellular traps” or NETs

34
Q

what does NET contain

A

chromatin and granule proteins (incl. enzymes to degrade

pathogen virulence factors)

35
Q

what do monocytes give rise to

A

tissue macrophages

36
Q

what do most macrophages arise from?

A

non-hematopoietic precursors!

37
Q

what are dendritic cells

A

a third type of phagocyte (related
to monocytes / macrophages) but specialised for
interacting with lymphocytes

38
Q

what do cytokines produced by macrophages cause and what happens to leukocytes as a result

A

dialiation of local small blood vessels

leukocytes then move to periphery of blood vessel as a result of increeased expression of adhesion molecules

39
Q

desribe the action of the monocyte

A

Monocyte binds adhesion molecules on vascular endothelium near sites of infection and gets chemokines signal
the monocyte migates into surrouding tissue
monocytes differentiates into a macrophage and migrates to the site of infection

40
Q

what are Cytokines and chemokines

A

The hormones of the immune system

41
Q

what do Cytokines and chemokines allow

A

communication between a variety of immune and non- immune cells

42
Q

names of Cytokines and chemokines

A

Mostly referred to as “interleukins” hence IL-1, IL-2, IL-3 etc,
but some use “functional names” e.g “tumour necrosis
factor” (TNF)

43
Q

what are chemokines

A

A further heterogeneous and complex family of small
molecular weight chemotactic cytokines are known as
“chemokines” (approx 30 also)

44
Q

Cytokines and chemokines regulation

A

• Mostly short acting “hormones” but can have systemic
effects e.g. in shock
• May be released in a polar fashion at “synapses”
• Recognised on target cells by specific receptors (with
some redundancy)
• Receptor expression is highly regulated to control the
targets and duration of response
• Subsets of cytokines / chemokines may be selectively coregulated
and help define cell subsets e.g Th1 and Th2
CD4+ lymphocytes

45
Q

Function of natural killer cells (an ‘innate’ lymphocyte

A 
Involved in tumour
surveillance
Kill “altered self” targets
Produce macrophage
activating cytokines e.g. IFNg
46
Q

what is at the head of a cytokine cascade responsible for symptoms
of rheumatoid arthritis

A

TNF

47
Q

TNF blockade may cause what

A

TB reactivation

- increased risk of secondary infection

48
Q

what do steroids affect

A

multiple aspects of immune

function, including cytokine release

49
Q

steroid affect on the immune system

A

steriod receptors are found in the cytoplasm complexed with a heat shock protein Hsp90
Steriods cross the cell membrane and bind to the steroid receptors complex releasing Hsp90
The steroid receptor complex can now cross the nuclear membrane
In the nucleus, the steroid receptors bind to specific gene regulatory sequences and activate transcription

50
Q

two example steriods

A

cortisol

prednisone

51
Q

Corticosteroid therapy of physiological effects

A

decreased inflammation caused by cytokines
decreased NO
Decreased prostaglandins and leukotrienes
Reduced emigration of leukocytes from vessels
introduction of apoptosis in lymphocytes and eosinophils

52
Q

Corticosteroid therapy of effect on

A

increased endonucleases
decreased adhesion molecules
decreased NOS

Block 4 ALS (7 decks)

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