c39 lec 8 and 9 Flashcards

1
Q

what is our first line of defense in our bodies (physical barrier to prevent infection)

A

skin

external barrier

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2
Q

our epithelial cells are coated in _____ to protect epithelium and prevent infection

A

mucus

thats why they are called mucosal surfaces/mucosa

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3
Q

most infections actually occur through _______ surfaces rather than our skin

A

mucosal surfaces

why?

mucosal surfaces has a much larger surface area = more immune cells

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4
Q

comprises all specialized lymphoid tissues for mucosal surfaces

A

MALT: mucosa-associated lymphoid tissues

  • GALT and other fall under MALT
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5
Q

the gastrointestinal tract is lined with

A

mucus and commensal bacteria

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6
Q

what does commensal bacteria do in our gastrointestinal tract?

A

helps us degrade and digest food

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7
Q

tonsils and adenoids (secondary lymphoid tissues) surround the entry point to the gastrointestinal and respiratory tracts

A

waldeyer’s ring

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8
Q

GALT stands for

A

gut associated lymphoid tissue

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9
Q

projections in the gut that aid in nutrient absorption

A

villi

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10
Q

what are the five benefits of commensal bacteria

A
  1. synthesize essential metabolites (ex. vitamin K)
  2. break down plant fibers in food
  3. inactivate toxic substances in food or made by pathogens (before our immune cells even see them)
  4. Prevent pathogens from benefiting from the resources of the human gut
  5. interact with epithelium to trigger development of secondary lymphoid tissue
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11
Q

____ dimers protect our mucosal surfaces (what type of immunoglobiulin)- MALT

A

IgA dimers

bring it in via transcytosis

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12
Q

receptor mediated transport from one side of a cell to the other

A

transcytosis

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13
Q

what maintains microbiome populations, keeps population growth in check (neutralize) and prevent it from overgrowing and infecting us

A

IgA

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14
Q

along with IgA what also protects our mucosal tissues

A

IgM

  • activated adaptive immune response constantly = consistent antibody production

as well as IgG: helpful in lower respiratory tract and urogenital tracts

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15
Q

do we have any complement pathway in mucosal tissues?

A

NOPE

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16
Q

made of glycoproteins, mucins (proteins), that provide viscous and protective features

A

mucus

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17
Q

very stick proteins that have simple sequence repeats

____ polypeptides are linked by disulfide bonds and form huge networks

sticky because of a lot of carbohydrate residues

A

mucins

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18
Q

secrete mucus

A

goblet cell

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19
Q

produce AMPs (Antimicrobial Peptides)

A

paneth cell

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20
Q

epithelial cells and lamina propria (connective tissue with immune cells and structures)

A

mucosa

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21
Q

bring antigens into the lumen of the intestines

A

M cells

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22
Q

specialized epithelial cells in GALT passing antigen from intestinal lumen to intestinal wall (lamino proprai)

A

M cells

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23
Q

help us constantly monitor the gut lumen

A

M (microfold) cells

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24
Q

M cells transport antigens to

A

peyer’s patch

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25
Q

can capture antigen from gut lumen by extending processes between intestinal epithelial cells

A

dendritic cells

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26
Q

disturbances to the environment cause

A

inflammation

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27
Q

for mucosal infections we don’t want

A

a lot of inflammation, not alot of requirement of immune cells because we mostly just use what we already have to deal with the problem

and don’t break down the tissue so no need to repair (repair causes a big immune response)

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28
Q

what are the two strategies that mucosal immunity employs?

A
  1. low inflammation: avoid tissue damage and prevent worse infections
  2. proactive: constantly producing an adaptive immune response towards commensal bacteria
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29
Q

intestinal macrophages are

A

non-inflammatory

  • they are phagocytic
  • do not contribute to inflammation, do NOT produce cytokines

inflammation anergic

but remember that intestinal epithelial cells create local inflammation

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30
Q

intestinal epithelial cells use ____ and _____ receptors to recognize bacteria that passed through mucus ….intestinal epithelial cells create local inflammation

A

TLRs and NOD

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31
Q

mucosal cells don’t do good with

A

inflammation

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32
Q

significant reduction of infection due to majority of population being immune

A

herd immunity

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33
Q

What are the types of vaccines (4):

A
  1. weaken the virus
  2. inactivate the virus (heat or chemically inactivate the virus)
  3. use part of the pathogen
  4. use part of the genetic code
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34
Q

live, weakened virus grown in non-human cells = strong immune response

not suitable for immunocompromised patients

A

live-attenuated viruses

35
Q

describe the new generation of the live-attenuated viruses

A

we delete the virulence gene and this makes it harder for the virus to revert to wildtype infectivity = safer for immunocompromised patients

36
Q

heat or chemically inactivating the virus is used for ______ patients

A

immunocompromised patients

requires multiple doses

36
Q

only uses the specific parts of a virus or bacterium that the immune system needs to recognize

A

protein subunit vaccines

  • no genetic material, cannot replicate = not as strong immune response
  • suitable for immunocompromised patients, requires multiple doses
37
Q

what is a type of subunit vaccine where protein is attached to carbohydrate to elicit an immune response

A

conjugate vaccine

38
Q

conjugate vaccines ( a type of subunit vaccine) uses what as the protein

A

toxoids (inactivated toxin)

39
Q

what makes a conjugate vaccine better than a polysaccharide vaccine?

A

it induces activation of Helper T cells

40
Q

how do vaccines against bacterial diseases differ from vaccines for viral diseases?

A

they target toxins instead

only bacterial vaccines target toxins because viral diseases don’t make toxins

41
Q

a modern approach to vaccine development that starts with analyzing the genome of a pathogen (like a bacterium or virus) to identify potential vaccine targets, rather than starting with the pathogen itself in the lab

A

reverse vaccinology, why we are able to come up with vaccines so fast

42
Q

increase the vaccination immune response

43
Q

can create a depot (storage) = slow, controlled release of vaccine

44
Q

may be added to a vaccine to mimic danger signals and catch the attention of the immune system

A

an adjuvant

45
Q

what do we not have a vaccine to yet?

A

HIV

  • it mutates so rapidly, integrates into host DNA and evades our immune system
  • attenuated vaccines are unsafe
  • our attempts to make a successful vaccine keep failing
46
Q

some HIV patients that manage the idsease better have

A

broadly neutralizing antibodies (BnAbs)

47
Q

for respiratory viruses, they are trying to replace muscular vaccines with _____ vaccines to trigger a mucosal immune response

A

intranasal vaccines

(up ur nose hole)

48
Q

what is one cancer vaccine that has been successful

A

gardasil vaccine to prevent HPV, prevent cervical cancer

49
Q

antigen-based cancer vaccines target

A

neoantigens

50
Q

prostate cancer vaccine in use in prostate cancer patients

51
Q

mutation allows for escape from _____

52
Q

yearly changes in influenza viruses: slow changes

A

antigenic drift

53
Q

outbreak within a population

A

epidemic

influenza viruses are typically epidemic

54
Q

fast changes in viruses

A

antigenic shift

55
Q

worldwide outbreak of infection

56
Q

co-infection results in an exchange of genetic information and generates more competitive virus

A

recombination

57
Q

ross link receptors together to trigger broad T cell activation

A

superantigens

58
Q

superantigens cross-linking receptors together to tripper broad T cell activation can lead to

Ex. 2-20% of T cells activated instead of 1 in 10 000

A

toxic shock syndrome

59
Q

have proteins that disrupt antigen processing and presentation on MHC class I proteins

60
Q

genetic process where one DNA sequence is non reciprocally copies over another, making them more similar or identical

A

gene conversion

61
Q

viruses that hide from our immune system

A

latent viruses

62
Q

_____ infection causes immune amnesia

63
Q

arise from absent or defective component in either innate or adaptive immunity

A

immunodeficiencies

64
Q

immunodeficiency inherited through genetics

A

primary immunodeficiency

65
Q

immunodeficiency due to environmental factors (ex. malnutrition, viral infection,etc)

A

secondary immunodeficiency

66
Q

microbes that do not affect healthy individuals but infect immunocompromised individuals

A

opportunistic infection

67
Q

what does HIV lead to

A

AIDS (acquired immunodeficiency deficiency syndrome)

68
Q

slowly depletes CD4 T cell population

69
Q

another name for mono or the kissing disease

70
Q

EBV (or mono or kissing disease) can trigger what

A

multiple sclerosis

71
Q

how an EBV infection trigger the development of Multiple sclerosis (MS)?

A

EBV has a surface antigen that is similar to a protein on the myelin sheath

when our bodies protect against EBV infection and get rid of EBV infected cells, we create B cells and T cells to do so

but since the surface antigen is similar to the protein on the myelin sheath, the T cells and B cells might target the myelin sheath and degrade that instead leading to MS

72
Q

how come immune responses to HIV rarely eliminates virus

A

due to rapid maturation rate = progression to immunodeficiency

73
Q

AIDS is a _______ immunodeficiency

74
Q

has helped majority of population of infected HIV individuals prevent progression to AIDS

A

anti-retroviral therapy (ART) / combination therapy

because we want to target all 5 stages of HIV development

75
Q

multiple anti-viral drugs

A

combination therapy or ART (anti-retroviral therapy)

76
Q

allows for increases T cell numbers and prevention of AIDS

A

anti-retroviral therapy (ART) or combination therapy

77
Q

HIV has ______ for viral entry

A

co-receptors (additional to CD4)

78
Q

initial HIV infections come from

A

R5 viruses (M-tropic)

79
Q

what are the two types of HIV viruses that can infect us

A

X4 virus : T tropic
X5 virus: M tropic

80
Q

why is the CCR5 mutation is beneficial for HIV infection

A

because those with this mutation don’t get R5 HIV infection!

because R5 binds to CCR5 and CD4

81
Q

X4 (t tropic) HIV virus binds to

A

CD4 and CXCR4

82
Q

R5 (m tropic) virus binds to

A

CD4 and CCR5