Innate immunity Flashcards

1
Q

what white blood cells are involved in the innate immune ?

A

macrophages and dendritic cells , neutrophils , basophils , eosinophils , mast cells and NK cells

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2
Q

there’s 4 main categories of physical barriers to limit entry of forgein pathogens what are they ?

A

anatomic
physiologic
phagocytic
inflammatory

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3
Q

describe anatomic ?

A

skin and mucous membranes

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4
Q

physiologic ?

A

temperature , low pH and chemical mediators

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5
Q

phagocytic ?

A

digestion of micro-organisms by a phagocytic cell.

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6
Q

inflammatory ?

A

vascular fluid leakage

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7
Q

describe what a breach to the barrier may look like ?

A

An insect bite or injury

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8
Q

what is released from the injured tissue and what does this lead too ?

A

a danger signal is released and this damage signal recruits complement components , antibodies , pro inflammatory mediators ,macrophages , lymphocytes and PMN’s from the vascular bed to the area of injury. These cells are all also recruited through the release of cytokines. These cells then exudate , this means there is a mass of cells and fluid that has seeped out of blood vessels. These damage then causes the activation of the endothelium and there is an increased permeability so the cells can reach the tissue.

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9
Q

what are PAMP’s ?

A

pathogen associated molecular patterns

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10
Q

what are PRR’s ?

A

pattern recognition receptors

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11
Q

what binds to the PRR’s?

A

the PAMP’s

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12
Q

what does this binding result in ?

A

causes the activation of innate cells such as macrophages and mast cells. The activation of these cells causes the release of inflammatory mediators that can recruit further innate cells and lymphocytes.

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13
Q

what’s the 5 symptoms of inflammation in greek and english ?

A
calor - heat 
rubor - redness 
tumor - swelling 
dolor - pain 
functi olasea - loss of funciton
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14
Q

what can PRR’s include ?

A

toll like receptors

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15
Q

give examples of TLR’s and their associated ligands ?

A

TLR1 - lipoproteins

TLR3 - dsRNA

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16
Q

what are TLR’s important in ?

A

pattern recognition

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17
Q

how does the mechanism work ?

A

the pathogens use similar molecules that are distinct from eukaryotes and these are the Pathogen associated molecular patterns ( PAMP’s) , it is through these PAMP’s that the pathogen is recognised.

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18
Q

what’s a consequence of TLR stimulation ?

A

often cell activation , the cells being activated will only be innate cells and no T or B lymphocytes as they are acquired immunity cells. For example cytokines and chemokines will be secreted which increases phagocytosis and intracellular killing.

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19
Q

will a macrophage express just one type of TLR ?

A

nope many so that it can respond to a range

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20
Q

what occurs if the bacteria binds to the TLR on the macrophage ?

A

the bacteria binds to the macrophage receptor via the PAMP’s this causes the release of cytokines and small lipid mediators of inflammation. After this is released the macrophage will engulf and digest bacteria to which they bind.

21
Q

what happens to the antigens entering the body ?

A

they are taken up by the APC where they are processed and shown on the cell surface as MHC peptide complexes

22
Q

how do cytokines affect the blood vessels ?

A

the tight junctions between the endothelium cells loosening which allows fluid to pass out from the blood vessels and cause local swelling. Leakage of RBC causes the local tissue to become reddened , the activated endothelium will express local adhesion molecules that allow phagocytes to migrate out of the blood vessel.

23
Q

what is delayed hypersensitivity response ?

A

this is a response to an antigen entering the body as above and it takes 1 to 3 days

24
Q

what is acidification ?

A

a low pH kills the pathogen

25
Q

toxic oxygen derived product ?

A

hydrogen peroxide

26
Q

toxic nitrogen oxides ?

A

nitroc oxide

27
Q

antimicrobial peptides ?

A

defensins and cationic proteins

28
Q

enzymes ?

A

lysozyme will dissolve the cell walls of some Gram + bacteria , acid hydrolyses will then further digest the bacteria.

29
Q

whats the steps to phagocytosis ?

A
  • Recognition
  • Pseudopod formation
  • Ingestion
  • Phagosome
  • Phagosome function
  • Digestion
30
Q

whats a cell called that carries out phagocytosis ?

A

phagocyte

31
Q

describe the stages ?

A
  1. Is when the chemotaxis and adherence of microbe to the phagocyte
  2. The TLR binds to the PAMP and the microbe is ingested
  3. The phagosome or phagocytic vesicle forms round the microbe trapping it in an intracellular vesicle.
  4. The phagosome then fuses with the lysosome to form a phagolysosome and it can deliver the enzymatic material inside the lysosome.
  5. The microbe is then digested by the enzymes
  6. The residual body forms which contains any indigestible material.
  7. The waste is then discharged from the cell
32
Q

what receptors is the phagocyte activated by ?

A

Fc receptors on the cell surface

33
Q

what are chemokines?

A

family of small cytokines that are involved in cell migration

34
Q

what is chemotaxin ?

A

the movement of a cell or organism that is induced by a chemical.

35
Q

is the selectin mediated adhesion to a leukocyte sialy lewis x weak or strong ?

A

weak

36
Q

what does this allow ?

A

the leukocyte to roll along the vascular endothelial surface.

37
Q

how does the selectin bind to the leuokocyte ?

A

via the siayl lewis X ligand

38
Q

how does the adhesion molecule slow down the blood cells ?

A

by using the selectins that bind to the lectins on the target cell and this is called rolling

39
Q

what occurs once the leukocyte has slowed down ?

A

other adhesion molecules can now be attached tightly such as LFA1 which is an integrin or CAM which is a cell adhesion molecule

40
Q

once bound the molecule will extravasate , what does this mean ?

A

it will pass through the endothelial cell lining and enter the blood vessel

41
Q

what occurs now ?

A

chemokine binding now signals the leukocyte to migrate along the chemokine concentration gradient. The source of inflammation is the source if chemokine concentration gradient.

42
Q

what is a complement ?

A

collection of serum proteins that are activated by a number of factors which in turn cause serial activation of proteases and this leads to several functional outcome.

43
Q

what is the classical pathway ?

A

involves antigen antibody complexes and this leads to complement activation and the recruitment of inflammatory and immunocompetent cells.

44
Q

lectin pathway ?

A

involves mannon binding proteins. complement and the opsonisation of pathogens occurs. Lectin is a molecular pattern. Results in membrane attack.

45
Q

alternative pathway ?

A

Bacteria activates the complement proteins

46
Q

what does complement lead to ?

A

cell recruitment , activation and opsonisation. C8 binds and this leads to insertion into the cell membrane where pores are made in the membrane and this leads to membrane lesions in the pathogen.

47
Q

what does the breakdown of the pathogen lead to ?

A

lots of antigens being generated ,these then represent the fragments of the various proteins expressed in the pathogen. These can then be recognised by the adaptive immune system.

48
Q

what is phagocytosis ?

A

The uptake of bacteria by an immune cell

49
Q

what are the TLR’s an example of ?

A

Pattern recognition receptor PRR.