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IMMUNOLOGY VDMP817 > lecture 4 > Flashcards

lecture 4 Flashcards

1
Q

function 1

A

recruited to inflammation site after neutrophil

- destroy any surviving microbes through oxidative/nonox mechanisms (finishers!)

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2
Q

function 2

A

phagocytose dead or dying neutrophils

- prevent any tissue damage that is caused by neutrophil enzyme

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3
Q

function 3

A

secrete cytokines/chemokines which initiates a local and systemic response

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4
Q

function 4

A

generate nitric oxide - powerful oxidizing agent

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5
Q

function 5

A

remove foreign particles from bloodstream and respiratory tract

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6
Q

function 6

A

initate repair of damaged tissues

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7
Q

function 7

A

essential antigen presenting cells (APCs) for the adaptive immune system

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8
Q

blood cell count

A

2-8 % of WBC - 0-800

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9
Q

monocyte properties

A
  1. round w kidney shaped nucleus
  2. phagosomes/lysosomes for phagocytosis and killing (not the best at monocyte stage)
  3. circulate 3 days then enter tissues
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10
Q

monocyte location

A 
bone marrow (myelopoesis)
blood (released from bone marrow to circulate)
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11
Q

monocyte function

A

recruited to the sites of tissue inflammation to become macrophages

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12
Q

macrophage properties

A
  1. derived from blood monocytes

2. phagosomes that contain killing chemical and proteins (higher than monocytes) - good!

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13
Q

macrophage location/subsets

A 
brain: microglial
connective tissue: histiocytes
lung: alveolar macrophages, intravascular macrophages 
liver: kupffer cell
lymph node: macrophage
spleen: macrophage
blood: monocyte
bone marrow: macrophage (osteoclast)
serosa: macrophage
dendritic cell!
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14
Q

macrophage function

A

key sentinel
express PRR to act as radar (eyes) to react and recombine pathogens
active phagocyte
trap and clear particulate matter from the blood circulation

can see from injected mouse that the liver and spleen macrophages take up particulate dye

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15
Q

bacterial/particle clearance from the blood

A

differs among species

kupffer cells (liver) and macrophages in spleen - dogs and rodents

lung pulmonary intravascular macrophages - cats, horses, ruminants, pigs

aerosol route - nose, tracheal cilia, bronchia and bronchioles, alveolar macrophages in lung

dermal route - antigen trapped by macrophages/dendritic cells of skin then migrate to lymph nodes (to training! nearest to site of infection) which will stimulate an adaptive immunity

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16
Q

M1 series

A

resting macrophage -> TLRs and related receptors (alarmins, cytokines etc) from inflammation -> innate activation (^ lysosomal enzymes, phagocytosis, membrane receptors, protease secretion) -> IFNg (through IL12 which stimulates NK to release IFg) -> classical activation of M1 (^ size, movement, membrane activity, lysosomal enzymes, phagocytosis, bactericidal activity, MHC class 2 expression, NO production!)

17
Q

M2 series

A

resting macrophage -> IL4, IL13, IL10 -> alternative activation (^ tissue repair, MHC class 2 expression, reduced microbial killing)

happens after M1s do their job when the inflammation is lower these come in!

18
Q

M1 o2 dependent killing

A

oxygen dependent (similar to neutrophil + NOS)

phagosome: NADPH oxidase - superoxide anion & H202
phagolysosome: NOS2 (oxidizes arginine to citrulline and NO! NO combines w superoxide anion to produce NO free radicals (BIG killers of microbial)

NOS2 is unique to M1

19
Q

M1 nonO2 dependent killing

A

natural resistrance associated macrophage protein (NRAMP) - M1 only
- transports divalent metals out of phagosome which inhibits the bacterias metabolic mechanism = death! and this is helpful if bacteria is resistant to NOS

lysozyme: proteolytic enzyme degrades cell wall
defensins (cationic peptides): makes holes in pathogen cell wall
acidic pump: add H+ ions and reduce pH

siderophore on bacteria and binds metals to keep to eat but NRAMP better!

20
Q

M2 function

A

clean up dying/dead neutrophils (die every 24 hrs)
produce protease inhibitors to neutralize the neutrophil enzymes (elastase)
produce growth factors (TGF, FBF)

neutrophils have increased number at the site of infection

21
Q

major macrophage surface receptors

A 
cytokine (CD25 - interleukin 2)
complement receptors (CR3/CD11b/18, CRI/CD35)
antibody receptors (CD16/FcgRIII, CD32/FcgRII, CD64/FcgRI)
transport receptors (CD71 - transferrin)
other (TLR2 & TLR4 - PAMPs, CD40)

complement receptors are well sutied to efficiently take up the opsonized pathogens
opsonization: antibody to FcgR’’ receptors which initiates the opsonization uptake

antibody and complement receptors injections decrease the bacteria in blood by 5ish minutes compared to no antibody the bacteria is never removed

22
Q

cytokine production by macrophage

A 
interleukin 23
interleukin 1
interleukin 6
interleukin 12
interleukin 18
tumor necrosis factor a

all are considered cytokine receptors

23
Q

IL23

A

cytokine produced by macrophage that stabilizes Th17 cells

24
Q

IL1

A

cytokine produced by macrophage that costimulates Th2 cells
stimulates acute phase responses

increases expression of selectins and integrins

25
Q

IL6

A

cytokine produced by macrophage that promotes B cell differentiation
stimulates acute phase responses

26
Q

IL12

A

cytokine produced by macrophage that costimulates Th1 cells

stimulates NK cells to release IFNgamma which activates macrophage!

27
Q

IL18

A

cytokine produced by macrophage that promotes IFNgamma production by Th1 cells - activating macrophages

28
Q

TNFa

A

cytokine produced by macrophage that is cytotoxic
stimulates Tcell growth
stimulates acute phase responses
triggers inflammation

enhance killing of virus/bacterial (LPS) infected cells and tumor cells by assembling NADPH oxidase!!
increase expression of selectins and integrins w IL1

29
Q

IL8

A

cytokine that is involved in local inflammation (w IL1 & TNFa) that attracts neutrophils through chemotaxis

30
Q

systemic inflammatory response from TLR4 macrophage as result of LPS

A

LPS is PAMPs that binds to TLR4 PRR on macrophage:

  1. IL1, TNFa, IL6 -> brain -> ^ prostaglandins (vasodilation and smooth muscle relaxation - inflammation) -> fever
  2. IL1, TNFa, IL6 -> liver -> acute phase proteins (leukotrienes can use this value to see if sick in blood)
  3. IL1, TNFa, IL6 -> effect bone marrow; ^ release & myelopoieses -> neutrophilia or _ erythropoiesis -> anemia
31
Q

TNFa biological actions at diff levels

A

low (<10^-9): local inflammation - endothelial cell has adhesion molecules and is producing IL1 and chemokines, leukocyte activation

medium: systemic effects - brain (prostaglandins - fever), liver (acute phase proteins), bone marrow (leukocytes released & decreased RBC)

high (>10^-7): septic shock - heart (low Q), blood vessel (low pressure w thrombosis and low resistance), liver (hypoglycemia - high sugar)

32
Q

acute phase proteins

A

positive: concentration in blood increases
- complement proteins (many functions; chemotaxis, vascular changes - takes care of business!)
- fibrinogen (blood coagulaent)
- serum protease inhibitors (dampen enzyme activity of neutrophils - elastase)
- iron binding proteins (lactoferrin! - tie up iron so bacteria cant nibble on it)
negative: concentration in blood decreases
- albumin (stabilizes blood, a decrease will disregulate blood and lower bp)
- transferrin (transports iron into tissues)

33
Q

endotoxic shock

A

bacterial endotoxin (LPS PRR) -> TLR4/CD14 on macrophage -> IL1, IL6, TNFa, CCL8, NO -> fever, acidosis, hypotension, complement activation, intravascular coagulation, endothelial damage (ACT ON VASCULAR ENDOTHELIUM) -> multiple organ system failure -> death

34
Q

toxic shock syndrome

A

macrophage is bound to Th cell by staphylococcus aureus toxins -> overproduction of IL2 & IFNgamma -> secondary overproduction of IL1 & IFNgamma -> rash, fever, hypotension, organ failure -> death

IMMUNOLOGY VDMP817 (22 decks)

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