Innate Immune System

Question 1

What are the six routes of entry?

Answer 1

airway 
GI tract 
GU tract 
External surface
Wounds and abrasions 
Insect bites

Question 2

what is the first phase of response to initial infection

Answer 2

innate immunity:

• immediate response
• 0-4 hours

Question 3

What is the second phase of response to initial infection

Answer 3

early induced response:

- 4-96 hours

Question 4

what is the third phase of response to initial infection

Answer 4

adaptive immune response:

>96 hours

Question 5

what are the three barrier to infection

Answer 5

chemical
mechanical
microbiological

Question 6

chemical barriers

Answer 6

• 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)

Question 7

mechanical barriers

Answer 7

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

Question 8

microbiological barriers

Answer 8

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

Question 9

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

Answer 9

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

Question 10

What are all cells derived from

Answer 10

hematopoietic cells

Question 11

monocyte

Answer 11

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

Question 12

what is another name for granulocytes

Answer 12

polymorphonuclear (PMN) leucocytes

Question 13

neutrophils

Answer 13

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

Question 14

eosinophils

Answer 14

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

Question 15

neutropenia

Answer 15

low number of neutrophils

may be genetic or the result of medication including chemotherapy

Question 16

Chronic Granulomatous disease

Answer 16

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

Question 17

alpha 1-antitrypsin deficency

Answer 17

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

Question 18

eosinophilia

Answer 18

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

Question 19

eosinopenia

Answer 19

often seen when glutocorticoids used

Question 20

basophils

Answer 20

function similar to mask cells and eosinophils 
- dark purple granules

Question 21

mast cells

Answer 21

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

Question 22

what are within the two divisions of lymphocytes

Answer 22

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)

Question 23

Natural killer cells

Answer 23

recognise virally infected cells non-specifically

Question 24

dendritic cells

Answer 24

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

Question 25

What do NK cells produce and what are the actions

Answer 25

- 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

Question 26

The key difference between NK and CD8 T cells

Answer 26

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

Question 27

What happens if a cell presents a MHC class1 receptor?

Answer 27

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

Question 28

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

Answer 28

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

Question 29

What are the two different types of complement pathway

Answer 29

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

Question 30

What are the further pathways of the these complement pathways

Answer 30

- recruitment of inflammatory cells - opsonisation of pathogens, facilitating uptake and killing by phagocytic cells - lysis and death of pathogens

Question 31

what is protein 3b

Answer 31

membran -binding protein and opsonin

Question 32

what are proteins C5a and C3a

Answer 32

they are peptide mediators of inflammation

Question 33

how is the classical pathway initiated

Answer 33

by activation of the c1 complex

Question 34

what causes the alternative pathway

Answer 34

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.

Question 35

role of C5a

Answer 35

C5a assists in the phagocytosis of C3b covered bacteria

Question 36

What proteins form the membrane attack complex

Answer 36

- 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

Question 37

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

Answer 37

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