Innate Immune System

Question 1

The immune system has two branches

Answer 1

Innate (natural) -born with

Adaptive (acquired) -acquire antibodies when exposed or vaccinated

Question 2

Major elements of the immune system

Answer 2

Soluble factors

cells

Question 3

difference between innate and adaptive immune system for soluble factors

Answer 3

Innate:
lysozyme, compliment, acute phase proteins, e.g. C-reactive proteins

Adaptive: antibodies

Question 4

differences for cells with innate and adaptive immune system

Answer 4

innate: phagocytes and Natural Killer Cells

Adaptive: T lymphocytes

Question 5

difference between innate and adaptive for first contact

Answer 5

Innate: same response each time
Non-specific, no memory, resistance not improved by repeated contact

Adaptive: second contact has a stronger response then the first contact
Specific, memory and resistance is improved by repeated contact

Question 6

list of innate defenses (8)
1-4 are biochemical
5-8 are chemical and physical

Answer 6

1) lysozyme in most tears, nasal secretions and saliva
2) sebaceous gland secretions
3) commensal organisms in gut and vagina
4) spermine in semen
5) mucous
6) cilia lining trachea
7) acid in stomach
8) skin

Question 7

innate immunity is always ______

Answer 7

present (not induced)

Question 8

two main mechanisms for innate immunity

Answer 8

limiting entry and limiting growth

Question 9

how does the skin limit entry into the host

what can a loss of skin lead to?

Answer 9

normally impermeable to majority of infectious agents
it is a hostile environment for many bacteria
lactic acid and fatty acid in sweat and sebaceous secretions aid to lower the pH

loss of skin for example do to a burn can lead to serious infections

Question 10

how do membranes limit entry into the host?

Answer 10

line the inner surface of the body and secrete mucus
inhibits bacterial adherence to inhibit entry

ciliary action -sweeping motion
remove microbes and other foreign particles

flushing action -tears/saliva/urine protect epithelial surfaces -presence of antimicrobial compounds

Question 11

what antimicrobial compounds can be present in flushing action of membranes?

Answer 11

Acids (gastric juices) -stomach
spermine and zinc in semen
lactoperoxidase (milk)
lysozyme in (tears, nasal secretions and saliva)

Question 12

how can the normal flora inhibit entry into the host?

Answer 12

-will compete or outcompete
Bacteria and fungi which are permanent residents on the body surfaces (skin and mucosal membranes)

suppress growth of pathogenic microbes:
protective layer
compete for nutrients
produce inhibitory compounds ->acids and collicins

Question 13

how does the body limit growth of pathogens that have entered the host

Answer 13

phagocytosis

soluble chemical factors (bactericidal enzymes)

Question 14

phagocytes include

Answer 14

macrophages

polymorphonuclear granulocytes

neutrophils=polymorphs

Question 15

how do Macrophages mature

where are they concentrated

Answer 15

promonocytes (in bone marrow) ->circulating blood monocytes -> mature macrophages (tissues)

concentrated in the lung, liver and lining of lymph nodes -well placed to filter off foreign material

Question 16

polymorphs

are the dominant...
share...
no...
\_\_\_dividing,\_\_\_\_lived, \_\_\_\_\_\_ nucleus
\_\_\_\_\_ cytoplasm

Answer 16

are the dominant white blood cell in the bloodstream
share common haemopoletic precursor ->myoblast
no mitochondria ->use glycogen for energy (anaerobic conditions due to inflammation, glycolysis is used when fighting infection
non-dividing, short lived, segmented nucleus
Granular cytoplasm

Question 17

The first step in Phagocytosis uses attachment by…

Answer 17

pattern recognition receptors

PAMPs: “pathogen associated molecular patterns” on microbe (e.g. LPS, proteins)
PRRs “pathogen recognition receptors” on phagocyte

Question 18

what happens when the PRR recognizes the PAMP

Answer 18

NFkB: Nuclear Factor Kapa beta cells and IRF: Interferon Receptors (different types) are activated to induce transcription products in phagocyte to kill pathogen

Question 19

the second step in phagocytosis is forming a phagosome after recognition of the PRR to the PAMP. how does this work?

Answer 19

the actin and myosin contractile system of the pseudopodia forms the phagosome

Question 20

what are the last two steps once the phagosome is formed?

Answer 20

Granule fusion/killing and then release of the microbial products

granule fusion and killing uses oxygen independent and dependent factors

Question 21

Phagocytosis and Complement system includes

Answer 21

contact-dependent
Formyl methionyl peptides attract leukocytes -chemotaxis -weak signal
compliment proteins

Question 22

the compliment system is

how are complement components designated?

Answer 22

cascade in which product of one reaction is enzymatic catalyst of the next

compliment (C’) components are designated “C” followed by a number e.g. C3, the most abundant an central component

Question 23

Soluble Chemical Factors of the complement system (Normal Plasma)

describe the feedback loop for the first step in the compliment system

Answer 23

C3 activation -> two breakdown products, C3b and C3a
C3b can complex with factor B (another C’ component)
C3bB is acted upon by an enzyme factor D to produce C3bBb
C3bBb aka C3 convertase which can split more C3 to C3a and C3b

Question 24

what decides if the compliment system moves on to the alternative complement pathway?

Answer 24

soluble C3 convertase is unstable and degrades
in presence of CHO/ other bacterial surface molecules, C3 convertase is no longer susceptible to breakdown
alternative complement pathway begins

Question 25

describe the steps in the alternative compliment pathway

Answer 25

C3b binds to microbial surface and acts as “opsonin”
C3b +C3 convertase act on next component C5
C5 is split into C5a and C5b
C5b becomes membrane bound and is joined by C6, C7, C8 and C9
together become inserted into the lipid layer of membrane and form membrane attack complex (MAC) ->cell lysis

Question 26

in the alternative complement pathway C5a and C3a cause mast cell degranulation -release of chemicals that mediate:

Answer 26

1) increased vascular /capillary permeability allows flow of fluid and plasma components to site of infection, part of “acute inflammatory response”
2) chemotactic attraction of polymorphs through blood vessel walls to C3b-coated bacteria because polymorphs have a receptor for C3b on the surface of bacteria so it will tightly bind and phagocytosis occurs

Question 27

Acute phase proteins

Answer 27

increased concentration in plasma response to injury and inflammation 
e.g. C-reactive protein 
mannose binding protein (MBL)
-bind to PAMPs
-fix complement and opsonize bacteria

Question 28

Antimicrobial Factors

Answer 28

Act within phagocytic cells but also in bodily fluids
tears in saliva (lysozyme)
lactoferrin (blood) -doesnt allow iron to be available for bacteria

Question 29

interferons (IFNs)

Answer 29

Discovered as a means of viral interference
cell infected with one virus resistant to superinfection with 2nd unrelated virus
infected cells secrete IFNs -bind to specific receptors on nearby uninfected cells
IFN causes cells to produce two types of enzymes that interfere with virus replication to limit spread

Question 30

Extracellular killing via NK cells

Answer 30

Bind to receptors on virus-infected cells causing NK activation and release of granules
e.g. perforin that insert into host membrane forming pore (like MAC)
allow entry of 2nd molecule, granzyme B that leads to apoptosis

Question 31

Extracellular killing via Eosinophils

Answer 31

combat large parasites -helminths (too large to be engulfed by phagosome)
bind to C3b (via C3b surface receptors) which cause activation
several toxic compounds released that damage membrane via hole formation