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Host Defense > Test 2, Deck 3 > Flashcards

Test 2, Deck 3 Flashcards

1
Q

where do osteoblast vs osteoclasts come from?

A

1) osteoblast- osteochondral progenitor from mesenchymal stem cell (also does adipocytes)
2) osteoclast- monocyte precursor (HSC)- can fxn as APCs

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2
Q

where is RANK expressed?

A

on pre-osteoclast and osteoclast

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3
Q

what ratio determines bone formation?

A

OPG/RANKL (both made by osteoblast)

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4
Q

aside from osteoblasts, what else secretes RANKL?

A

B&T lymphocytes, neutrophils, monocytes, DCs

- overwhelms the OPG capacity, get bone breakdown

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5
Q

which cytokines induce RANKL and promote osteoclasts?

A

IL-1, 6, 8, TNFalpha and IL-17** the arthritis one

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6
Q

which cytokines inhibit OC differentiation and proliferation?

A

IL-4, 10

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7
Q

what happens in rheumatoid arthritis?

A
  • something triggers DCs to release Il-23
  • neighboring cells contribute Il6, TGFbeta
  • Th17 infiltrates synovium, produces IL-17
  • get activation of osteoclasts and activation of neutrophils
  • is pro-bone loss, lose joint function
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8
Q

what is a good treatment option for rheumatoid arthritis?

A

use monoclonal antibodies to block excess RANK-L (act like OPG), decrease osteoclast activation

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9
Q

two major types of macrophages

A

M1- proinflammatory

M2- anti-inflammatory

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10
Q

pro-inflammatory cytokine and potente chemotactic signal for monocytes/macrophages in WA, derived from macrophages

A

osteopontin

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11
Q

other important cytokines produced by adipocytes and whether they are pro/anti inflammatory

A
  • leptin - pro-inflammatory
  • (resistin- inhibits adiponectic, pro-inflammatory, derived from macrophages)
  • visfatin- pro-inflammatory, pro-angiogenic
  • adiponectin- anti-inflammatory
  • macrophage inhibitory cytokine- promotes adiponectic
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12
Q

do you want a predominance of M1 or M2 macrophages? what do they up regulate?

A

M2
increase IL-4, 10 and NfkappaB
anti-inflammatory milieu

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13
Q

what is the most potent monocyte attractant secreted by adipocytes?

A

CCL2

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14
Q

what happens to the type of macrophages with obesity and how?

A
  • increase the size of adipocytes, results in pro-inflammatory milieu
  • adipocytes release CCL2 which attracts monocytes
  • macrophages are M1, can initiate paracrine loop to make recruited monocytes M1 & recruit more monocytes
  • portal vein drains fat & pro-inflammatory cytokines, goes to liver
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15
Q

how is the innate response suppressed in the CNS?

A

microglia + IL-10 + TGFbeta

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16
Q

two types of microglia in CNS

A

1) migrate early, acts like M2 macrophages, highly branches (like DCs), display little MHC
2) perivascular, derived from circulating monocytes

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17
Q

how does neuroinflammation occur?

A
  • activation of perivascular glial cells by DAMPs and PAMPs
  • become M1s, secrete pro-inflammatory cytokines
  • lose neurons (IL-6 especially bad)
  • can cause delirium
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18
Q

where are sites that polymorphism can occur and dictate the host response?

A
  • MHC molecules (how they present antigen)
  • TLR (controls type of immune response)
  • cytokines (differences in production)
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19
Q

T/F MHC can determine susceptibility or protection

A

TRUE- susceptibility to diabetes

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20
Q

The duration/intensity of a response depends on

A

how much a TLR is triggered

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21
Q

Vaccinogenetics- differences in response

A

1) Normal T&B cell response, induces active immunity
2) React to vaccine with hyper B/T cell response secondary to manner of MHC/TLR presentation+ cytokine polymorphism
3) no immune response b/c of MHC/TLR lack of effective presentation/activation/cytokine suppression

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22
Q

central rule of vaccinogenetics

A

widespread infection of a population results in a wide spectrum of antigen presentation to polymorphic TLR and cytokine genes that then dictate the clinical manifestations/ course of the disease

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23
Q

ground rules for vaccinogenetics- types of responses matched with types of disease/syndrome

A

TMMI- intracellular
IL17- fungal infections
B cells- toxins/organisms resistant to phagocytosis
T&B cells- viruses

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24
Q

what an adjuvant?

A
  • provides a way for slow antigen exposure (slow release)
  • induces innate immunity by activating TLRs
  • Alum does TH2 stimulation
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25
Q

if immune system could detect tumors, how would it response?

A

1) tumor presents antigen in MCH1, recognized by CD8/NK cells
2) B cell runs into antigen, activates Th2s, produces antibodies to antigens in cell wall, activates complement system and NKs with FcRs
3) APC runs into antigen, activates TMMI, macs kill tumor

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26
Q

how do tumors thwart activation of cytotoxic response?

A
  • convert infiltrating cells into Tregs OR inactivates them
  • secretes immunosuppressant cytokines
  • alters cell signaling
27
Q

which cytokine is secreted by tumors to convert T cells into Tregs?

A

CCL21

28
Q

what responses do Tregs block? what’s left?

A

block CD8+, B cells, CD4s

leaves NK cells

29
Q

what do tumors upregulate on their surface to paralyze/kill T cells?

A

PDL-1

PD-1 receptor is ON t-cells

30
Q

what happens when you inhibit PDL-1 with a MAB?

A

inhibits the “death” signal, allows CD8 cell to kill

31
Q

describe immune checkpoint therapy

A
  • use MAB to block CTLA4 (signal that turns T-cell off)
  • use MAB to block PD-1receptor and PD-L1
  • CD8+ cells won’t turn themselves off and won’t be killed by tumor cell!
32
Q

what cytokine can increase the epxression of PDL-1 on tumor cells?

A

INF-gamma

33
Q

direct connection between the CNS and the immune pathway? indirect?

A

direct: innervation of primary and secondary lymphoid organs + adrenal medulla
indirect: hormones

34
Q

what neuropeptides/neurotransmitters do stressors cause the release of? what do they stimulate? ** check

A

Epi/NE
GABA
Ach
serotonin

stimulate release of CRH from PVN

35
Q

which lymphoid tissues are stimulated by noradrenergic fibers? cholinergics? peptidergic?

A

noradrenergic secreting NE: bone marrow, thymus, spleen, lymph nodes
cholinergics secreting Ach: thymus
peptidergic secreting neuropeptides: thymus and lymph nodes

36
Q

connection between hypothalamus and adrenal medulla?

A

hypothalamus activates splanchnic which stimulate chromaffins of adrenal medulla to secrete catecholamines (Ne/E)

37
Q

what do immune effector cells (NLMEB) possess receptors for?

A

catecholamines, ACh, neuropeptides

38
Q

what do catecholamines (Ne/E) do?

A

increase leukocyte mobilization, increase NK cell activity; involved in fight or flight

39
Q

where are endorphins and enkephalins produced? what do they do?

A

endorphins- from POMC in pituitary after CRH stimulation, happiness/analgesia (hormone)
enkephalins- all over brain/adrenal with Ne/E, same receptors as endorphins (NTs)

both increase T cell reactivity and NK cell activity

40
Q

with acute, controllable emotional or mental stress, you see elevated

A

heart rate
cortisol
Ne/E

41
Q

what happens to leukocytes right after you jump? and hour later?

A

immediate: circulating NK increase cells due to increased catecholamines
1 hour later: circulating mononuclear cells decrease because cells have localized to lymph nodes (catecholamines and cortisol)

42
Q

what cellular mechanisms result in the redistribution of high circulating NK cells to the lymph nodes?

A
  • hormonal modification of adhesion molecules - aka increased CD11a
  • activation of its (CD11a’s) cognate on endothelial cells (ICAM-1)
43
Q

differences between types/amounts of stress on DHT (TMMI) response

A

** low cortisol from acute stress- enhances TMMI
high cortisol from acute stress- depresses TMMI
** chronic stress- decreases TMMI & leukocyte mobilization

44
Q

alzheimer’s caregivers exhibited

A

1- decreased cytokine production (IL1)
2- decreased antibody production
3- increase in the number of colds

45
Q

what cytokines induce “sickness behavior” by having a direct effect on the CNS- fever, headache, muscle and joint pain, diminished appetite, lethargy

A

IL1, Il6, TNFalpha

46
Q

where is the cholinergic anti-inflammatory pathway?

A
  • prevents excessive production of cytokines resulting in systemic inflammation
  • splenic nerve releasing NE on T-cells in spleen
  • T-cells released Ach, which acts on macrophages and inhibits transcription of inflammatory factors (IL1,6,8, TNF)
47
Q

describe the adaptive (energy saving) response to short term stressors

A
  • immediate release of catecholamines which mobilize leukocytes
  • immune system then temporarily suppressed by slower release of cortisol (maximizes energy for fight or flight)
48
Q

what does acute stress do?

A

1) greater leukocyte infiltration
2) enhanced production of chemokines to attract leukocytes
3) IL1, 6, TNF alpha
4) enhances maturation and trafficking of dendritic cells
5) promotes activation & recruitment of t lymphocytes, enhancing immunologic memory

49
Q

response to influenza virus

A

all of the immune responses:
innate : cytokines and NK cells and neuts and macs
adaptive: specific CD8+s, antibodies (+ complement), interferons

50
Q

response to candida albicans (fungi)

A

cytokine-activated phagocytes
- binds MBL to activate the lectin pathway of the complement system; once C3b is bound, it acts as powerful opsonin for phagocytosis

51
Q

response to streptococcus pnemoniae (extracellular bacteria)

A
  • have to produce antibody to anti-phagocytic capsule + activate complement
52
Q

response to neisseria meningitidis (gram-negative extracellular bacteria)

A

antibody and complement (b/c gram negative, can be lysed by MAC), phagocytosis

53
Q

response to clostridium tetani

A

antibody to spores

54
Q

response to mycobacterium tuberculosis (intracellular bacteria)

A

CD4+ tcells (Th1’s that activate macrophages by the production of cytokines) (antibody ineffective)

55
Q

response to schistosoma mansoni (parasite)

A

antibody directed complement attack, ADCC mediated by eosinophils (innate immunity is ineffective)

56
Q

antiviral effect of interferons

A

stimulate synthesis of 2 enzymes: synthetase and protein kinase

  • synthetase: makes long chain of adenines which activates ribonuclease to degrade viral mRNA
  • protein kinase: phosphorylates EIF-2, which inhibits the initiation complex for protein synthesis and viral mRNA is degraded
57
Q

where do the interferons come from and what do they target?

A

alpha- from leukocytes, target viral infected cells
beta- from any cell, target viral infected cell
gamma- DIFFERENT- from t lymphocytes and activates macrophages

58
Q

T/F Antibodies neutralized toxins produced by viruses

A

False- toxins are only produced by bacteria

59
Q

time course of primary vs secondary antibody response

A

IgM detectable at about 3-4 days , peaks between 2-3 weeks

IgG delayed 5-7 days, persists longer

60
Q

anti-viral but not anti-bacterial mechanisms

A

CTLs recognizing viral peptides
NKs finding viral infected cells
Interferons targeting non-viral cells

61
Q

T/F Neutralization by antibody binding is a strategy for targeting bacteria and viruses

A

false- only anti-bacterial toxins (but antibodies can be used to promote lysis/phagocytosis of virally infected cells)

62
Q

which cytokine is important to induce class switch to IgE?

A

Il-13

63
Q

which cytokine is important for the activation of eosinophils?

A

Il-5

Host Defense (6 decks)

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