immune system I - innate immune system Flashcards

1
Q

whats the sequence of events in inflammation that lead up to phagocytosis?

A
  1. defence by resident macrophages
  2. localised vasodilation
    3.increased capillary permeability
  3. localised oedema walling
  4. walling off of the inflamed area
  5. emigration of leukocytes
  6. phagocytosis
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2
Q

step 2: how is localised vasodilation induced and what happens in it

A

induced by mast cells degranulation
1.immediate arteriole dilation
2. increased local blood supply
3. increased number of phagocytes and plasma proteins

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3
Q

step 2: what happens when capillary permeability increased

A
  1. histamine-induced widening of capillary pores
  2. escape of plasma proteins
  3. increased osmotic pressure
  4. escape of accompanying fluid
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4
Q

step 4: what happens in localised oedema and what are the consequences?

A
  1. excessive fluid accumulation
  2. leads to localised oedema = swelling

consquences:
-increased distance between blood and cells so decreased diffusion rate of nutrients, o2 and waste hence reduced supply

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5
Q

in step 5 what happens in walling off of the inflamed area

A
  1. leaked plasma proteins are exposed to tissue so clotting and anticlotting factors of fibronectin are leaked
  2. fibrinogen is the final factor
  3. fibrin forms clots around the invader and or damaged cells to prevent spread of invader or toxic products
  4. inflamed area is walled off
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6
Q

step 6 what happens in emigration of leukocytes?

A
  1. in migration and adhesion, CAMs and integrins mean leukocytes are concentrated next to endothelial cells
  2. diapedesis where leukocytes squeeze through capillary pores
  3. chemotaxis occurs
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7
Q

how does target recognition in phagocytosis occur?

A
  1. surface characteristics such as roughness
  2. bacterial cell components - saccharides
  3. chemical mediator coats of opsonins such as C3b
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8
Q

what are the steps of phagocytosis?

A
  1. phagocyte membrane binds to bacteria
  2. releases the oxygen radicals of O2-.,OH., O and the cell surface membrane and in inner phagosome
  3. phagosome and the lysosome fuse
  4. discharge of acid and bactericidal enzymes
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9
Q

what are the bactericidal mechanisms of phagocytes?

A

-reactive oxygen intemediates
-lethal acidity in phagolysosomes
-lysozyme
-lysosomes contain lethal cationic proteins like lactoferrin
-catalase
-glutathione peroxidase

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10
Q

what happens to phagocytes as a result of their bactericidal mechanisms?

A

-accumalate toxic by-products
-lysosomal chemical release of cytosol causes phagocyte death
-pus production which is a collection of phagocytes, liquefied necrotic tissue and bacteria

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11
Q

what are the detrimental effects of phagocytosis?

A
  • pus causes tissue destruction to bacteria spread and painful
    -liberation of phagocyte lysosomal enzymes causes cell destruction and inflammation
    -certain intracellular organisms thrive inside macrophages causing satellite infections such as TB and leprosy
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12
Q

which leukocytes undergo exocytosis and how

A

macrophages, eosinophils and neutrophils
1. flattening of cell membrane towards the large enemy
2. fusion of lysosomal and cell membranes
3. spit out oxygen free radicals/ lysosomal enzymes

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13
Q

what do natural killer cells do and how do they undergo exocytosis?

A

immediate, non-specific destruction of virus-infected/ cancer cells

exocytosis:
1. attach via lectins to enemy target
2. exocytose perforin onto cell surface
3. membrane puncture
4. cell lysis or induced apoptosis of infected cell

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14
Q

give 3 features of interferon

A

-nonspecific resistance to viral infections
-interferes with viral replication
-1st line of viral defence

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15
Q

how does interferon reinforce other immune activities?

A
  1. enhances macrophage activity
  2. stimulates antibody production
  3. suppresses cell division - tumour growth
  4. enhances NK cell and cytotoxic T cell function
    overall forms anti viral and anti cancer effects
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16
Q

what is complement system?

A

a response thats either non specific or specific that complements the action of antibodies

17
Q

go over complement system and its pathway

A

ok

18
Q

where does complement system come from?

A

plasma proteins produced in liver that circulate in the blood

19
Q

give 3 plasma derived mediators of inflammation

A

-kalikrein-kinin system
-clotting and fibrinolytic systems
-complement system

20
Q

give 5 cell derived mediators of inflammation

A

-arachidonic acid derivatives like prostaglandins and leukotrienes
-platelet activating factor
-cytokines, lymphokines and monokines
-vasoactive amines: histamine, serotonin
-nitric oxide

21
Q

how does the hagemann factor XII activate the plasma derived mediators of the 1. clotting and fibrinolytic system and the 2. complement system

A
  1. -activates clotting cascade and plasminogen creating plasmin which causes fibrinolysis and degradation products to be formed
    -this changes vascular permeability
  2. -opsonin Cb3 creates the membrane attack complex
    -forms anaphylatoxins and this produces chemotaxins, enhances phagocytosis, smooth muscle contraction, and increases vascular permeability
22
Q

what does the activation of kallikrein system do?

A

reinforces histamine induced vascular changes and so positive feedback means new neutrophils trigger kallikrein

23
Q

give 6 features of platelet activating factor

A

-produced by all activated inflammatory, endothelial, injured cells
-stimulates own release
-potent inducer of platelet aggregation
-vasoactive mediator in dilation and permeability
-acts as a chemo attractant
-augments productions of mediators including AA metabolites

24
Q

give the two key features of chronic inflammation

A

-infiltration with mononuclear cells
-repair via angiogenesis and fibrosis

25
Q

what are the two types of granuloma

A

-collections of epithelioid cells surrounded by lymphocytes
-fused macrophages

26
Q

what cells are associated with chronic inflammation and may be associated with chronic inflammation?

A

lymphocytes, eosinophils, fibroblasts

27
Q

name 7 chronic inflammatory diseases

A

-TB
-leprosy
-syphilis
-sarcoidosis
-Crohn’s disease
-rheumatoid arthritis
-systemic lupus erythematosus
-multiple sclerosis