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Y1S2 > Innate Immune System > Flashcards

Innate Immune System Flashcards

1
Q

What are the six routes of entry?

A 
airway 
GI tract 
GU tract 
External surface
Wounds and abrasions 
Insect bites
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2
Q

what is the first phase of response to initial infection

A

innate immunity:

  • immediate response
  • 0-4 hours
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3
Q

What is the second phase of response to initial infection

A

early induced response:

- 4-96 hours

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4
Q

what is the third phase of response to initial infection

A

adaptive immune response:

>96 hours

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5
Q

what are the three barrier to infection

A

chemical
mechanical
microbiological

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6
Q

chemical barriers

A
  • fatty acids not he skin
  • enzymes (lysozyme) in the saliva, sweat and tears.
  • low pH in the stomach
  • antibacterial peptides such as defensives (skin and gut) and cryptidins (gut)
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7
Q

mechanical barriers

A
  • tight junctions between cells which prevents access
  • air and fluid flow across the epithelium
  • movement of mucus by cilia
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8
Q

microbiological barriers

A

normal flora compete for nutrients and attachment (biofilms), and also produce antibacterial substances (colicins)

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9
Q

what kind of receptors help to enhance the function of macrophages and monocytes

A
  • mannose receptor
  • glucan receptor
  • scavenger receptor
  • CD14 (LPS)
  • CD11b/CD14 (CR3)
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10
Q

What are all cells derived from

A

hematopoietic cells

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11
Q

monocyte

A

bilobed
large cells approximately 10 microns
becomes a macrophage when it enters the tissue
- phagocytosis and activation of T cells and initiation of immune response

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12
Q

what is another name for granulocytes

A

polymorphonuclear (PMN) leucocytes

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13
Q

neutrophils

A

70% of all WBC
multinucleated (lots of lobes)
- phagocytosis and killing of microorganisms
short time spent in circulation

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14
Q

eosinophils

A 
2% of all white blood cells 
filled with granules and is bilobed 
- killing of antibody-coated parasites through release of granule contents 
histamine, peroxidase, lipase
circulate for 12 hours
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15
Q

neutropenia

A

low number of neutrophils

may be genetic or the result of medication including chemotherapy

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16
Q

Chronic Granulomatous disease

A

failure in respiratory burst, superoxide production limited, antibacterial activity impaired

17
Q

alpha 1-antitrypsin deficency

A

elastase from neutrophils not adequately inhibited, excessive tissue damage during inflammation-pulmonary emphysema

18
Q

eosinophilia

A

increase in eosinophils, seen in parasitic infection of the gut, some vascular diseases, Hoskins disease, Addisons disease

19
Q

eosinopenia

A

often seen when glutocorticoids used

20
Q

basophils

A 
function similar to mask cells and eosinophils 
- dark purple granules
21
Q

mast cells

A

lots of granules appear very dark with light nucleus

  • when activated they release alot of substances that effect vascular systems
  • expulsion of parasites from the body through the release of granules containing histamine and other active agents
22
Q

what are within the two divisions of lymphocytes

A 
B AND T cells 
the adaptive immune response:
- B cells producing antibodies 
- T cells becoming helper T cells (CD4)
- T cells becoming cytotoxic T cells (CD8)
23
Q

Natural killer cells

A

recognise virally infected cells non-specifically

24
Q

dendritic cells

A

bridges the innate immune system and adaptive immune responses.
- specialised in antigen uptake and antigen presentation

25
Q

What do NK cells produce and what are the actions

A
  • induce resistance in viral replication in all cells
  • increase MHC class 1 expression and antigen presentation in all cell s
  • activates NK cells to kill virus-infected cells
26
Q

The key difference between NK and CD8 T cells

A

NK cells are not antigen specific. Also they do not require to undergo the lengthy clonal expansion of T cells in lymph nodes when virus is detected

27
Q

What happens if a cell presents a MHC class1 receptor?

A

it send a NO KILL signal and therefore the NK cell leaves it alone and continues to monitor elsewhere

28
Q

what happens there is no MHC receptor presented (therefore is a virus infected cell)

A

Sends a KILL ME signal and therefore the NK cells is activated to degrade the cell

29
Q

What are the two different types of complement pathway

A

classical pathway = antigen binds to specific antigen on pathogen surface
alternative pathway = pathogen surface creates local environment conclusive to complement activation

30
Q

What are the further pathways of the these complement pathways

A
  • recruitment of inflammatory cells
  • opsonisation of pathogens, facilitating uptake and killing by phagocytic cells
  • lysis and death of pathogens
31
Q

what is protein 3b

A

membran -binding protein and opsonin

32
Q

what are proteins C5a and C3a

A

they are peptide mediators of inflammation

33
Q

how is the classical pathway initiated

A

by activation of the c1 complex

34
Q

what causes the alternative pathway

A

caused by spontaneous hydrolysis (tickover) of serum C3, which then bind factor B allowing cleavage by factor D into Ba and Bb. The resulting soluble C3 convertase cleaves C3 to C3b, which binds to membranes.

35
Q

role of C5a

A

C5a assists in the phagocytosis of C3b covered bacteria

36
Q

What proteins form the membrane attack complex

A
  • C5b binds C6 and C7
  • C5b, 6, 7, complexes bind to the membrane via
  • C8 then binds to this complex and inserts into the cell membrane
  • C9 molecules then bind to the complec and polymerise
    this punches a hole in the bacterial surface therefore resulting in the spilling out of its contents which inevitably leads to death
37
Q

What are some examples of proteins which inhibit the membrane attack complex formation

A

DAF: Decay accelerating factor
MCP: membrane cofactor protein
CR1: complement receptor 1

Y1S2 (73 decks)

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