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Block 6 Week 1 > B Cells and Humoral Immunity > Flashcards

B Cells and Humoral Immunity Flashcards

1
Q

(blank) is a state of severe hypertension and spasticity in which an individual’s head, neck and spinal column take a complete “bridging” or “arching” position. This posture is caused by spasm of the axial muscles along the spinal column.

A

opisthotonus

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2
Q

(blank) is a highly fatal disease of humans. Mortality rates reported vary from 40% to 78%. The disease stems from a potent neurotoxin produced when spores germinate and vegetative cells grow after gaining access to wounds. The organism multiplies locally but symptoms appear remote from the infection site.

A

Tetanus

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3
Q

What is the causative agent of tetans?

A

clostridium tetani (found in heavily manured soil and GI of animals)

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4
Q

Why is tetanus vaccination so important?

A

because natural recovery from this disease is unlikely because it doesnt ellicit an immune response, you just die

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5
Q

In humoral immunity, what are the effectors of protection?

A

antibodies

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6
Q

How can you distinguish between humoral vs. cellular immunity?

A

adoptive transfer tests

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7
Q

(blank) is transferred by serum containing antibodies or by antibodies aone ( rattle snake venum, tetanus toxoid)

A

humoral immunity

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8
Q

(blank) is transferred only by cells (usually done in completely inbred mice or rats)

A

cellular immunity

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9
Q

How is humoral immunity transferred?

A

by serum containing antibodies by antibodies alone.

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10
Q

If you are transfering humoral immunity wthin a species, what happens?

A

they are accepted as self and are considered effective

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11
Q

What happens if you transfer antibodies across species?

A

antibodies last 5-7 days because they are immunogenic (elicit an immune response)

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12
Q

Is the transfer of antibodies awesome? why?

A

yes because it is practical and safe. Antibodies are human “self” and Ig can be irradiated to prevent viral infection

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13
Q

What is this:

an immune response that is not elicited by antibodies but rather antigen sepcific T cells and is tranferred only cells.

A

Cellular immunity

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14
Q

Why cant you really transfer T cell immunity?

A

because its hard to match MHC I and MHC II antigens and if they are not matching those cells will be killed

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15
Q

What three things influence humoral immunity?

A

amount of antigen, route of natural or prophylactic immunization, use of adjuvants

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16
Q

How long do specific antibodies live?

A

maintained for life, although concentrations drop slowly.

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17
Q

The affinity and concentration of an antibody is sometimes critical. Explain this as a priniciple for tetanus toxin/

A

antibodies for tetanus toxin nee to have an extremely high affinity and concentration in order to out-compete the toxin, this is why the tetanus vaccine is repeated.

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18
Q

What are immunogens?

A

molecules that elicit an antibody response

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19
Q

What are some common immunogens?

A

proteins > 25 micrograms (toxoids), killed pathogens, live attenuated viruses, conjugate and DNA vaccines.

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20
Q

What are adjuvants?

A

something that is added to improve immunizations but it itelf is not immunogenic.

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21
Q

What can adjuvants activate?

A

they can activate macrophages to secrete IL-1 and TNF alpha to activate helper T and B cells AND they keep immunogens localized

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22
Q

Routes of administration of vaccine or immunization affects the types of antibody made.
intramuscular?
Oral or intranasal?
IV?

A

IgG
IgA
poor route of immunization

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23
Q

If you repeatedly expose someone to a antigen what will happen?

A

you will increase the quantity and affinity of IgG and IgA

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24
Q

(blank) is a measurement of the binding strength of Fab antigen-biding site for its single antigenic epitope.

A

affinity
expressed as Ka=1/Kd
(ka= affinity, Kd= concentration to fill half the binding sites)

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25
Q

(blank) is a measurement of the total combined binding strength of a complete immunoglobulin molecule for a complex antigen that contains repeating epitopes.

A

avidity.
(think of this like velcro, one tooth of velcro wont have any strength, but numerous teeth of velcro create a very strong connection)

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26
Q

Explain how you can have low affinity but high avidity

A

an IgM antiody molecule with low affinity for a particular antigen (but that has 10 antigen binding sites) will bind with high avidity to a complex antigen that contains repeats of the epitope

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27
Q

(blank) becomes medically important for IgM and IgA because bacteria and viruses have repeating epitopes and proteins in the membranes, flagella, and capsules

A

avidity

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28
Q

WHy is antibody super important for botulin toxin, ebola virus, and tetanus?

A

Because these are very lethal in small concentrations so you must have high affinity to be able to bind even the smallest dose. (need to outcompete toxin for binding site)

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29
Q

How do you classify an immunoglobulin?

A

5 classes denoted by english letter (A-E)
Greek letters to describe heavy chains AND
Numbers for the isotypes
2 for IgA
4 for IgG
2 types of light chains called Kappa and Lambda

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30
Q

How many J chains are there for every polymeric unit (i.e immunoglobulin)

A

1 (think of it like a clasp of a necklace)

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31
Q

How do you determine the molecular weight of a immunoglobulin?

A

multiply each repeate by 150,000. (important because determines whether it can get out of the blood into tissues. greater than 50,000 cant get out of the kidneys, things that are smaller can.

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32
Q

How many antigen bining sites are on a pentameric Ig?

A

10, times each unit by 2

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33
Q

What is the first antibody made in immune responses and appears right after antigen is introduced?

A

IgM

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34
Q

Does IgM have a low or high affinity for antigens?

A

low affinity, but potential for high avidity

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35
Q

What is the serum concentration of IgM?

A

1.2 mg/ml

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36
Q

What is the serum half life of IgM?

A

about 5 days

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37
Q

What is the function of IgM?

A

fixes complement extremely well. Just 1 IgM antiboy on a bacterium can start complement killing

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38
Q

Is IgM made for life?

A

nope, it is termporary and tells you if you have had a recent infection or not

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39
Q

Where can you find IgM?

A

in secretions :)

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40
Q

What size is an IgG?

A

150Kd

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41
Q

How many binding sites does IgG have?

A

2

42
Q

What are the differences among the 4 classes of IgG?

A

AA seq of the IgGs differ in constant regions, hinges

43
Q

What is the second antibody made in the immune response and how long does it last?
What is its struture

A

IgG
persists for life
monomer so only has 2 binding sites

44
Q

Does IgG have a high or low affinity for antigen

A

high affinity

45
Q

What is the serum concentration for IgG?

A

7-12 mg/ml

46
Q

Which kinds of IgG have long half lives (21-24 days)?

A

IgG1, IgG2, IgG4

47
Q

Which kind of IgG has a short half life (7-8 days)?

A

IgG3

48
Q

What does IgG1 and IgG3 do?

A

fix complement

49
Q

HOw can you start a complement cascade with IgGs?

A

you need 2 of them close together

50
Q

What does IgG1 and IgG3 support?

A

antibody-dependent cell mediated cytotoxicity (ADCC)

51
Q

(blank) crosses the placenta to provide neonatal protection

A

IgG

52
Q

Whydo babies start getting sick around 6 months of age?

A

because the half lives of the immunoglobulins has pretty much depleted the IgG (passive immunity) that was given to the baby by its mother

53
Q

What is the structure of IgA?

A

it can be a dimer or trimer

54
Q

What is the weight of IgA?

A

dimer-300

trimer-450 Kd

55
Q

What are the 2 subclasses of IgA?

A

IgA1 and IgA2

56
Q

What is the number of antigen binding sites?

A

4 or 6

57
Q

Where do you find IgA?

A

in plasma and in secretions including breast milk, gut, tears, saliva, vagina

58
Q

Since IgA is passed through breast milk, how does this help the baby?

A

it doesnt because IgA just remains in the babys gut and does not enter the babys circulation

59
Q

What is the serum concentration and half life of IgA?

A

around 2 mg/ml

about 6 days

60
Q

What is the function of IgA?

A

to block pathogens at mucosal sites, their adhesion, their attachment to the gut wal

61
Q

How is IgA transported?

A

through eptihelial cells into mucosal secretions via secretory component

62
Q

What is the secretory component?

A

it is the tranport receptor for IgA

63
Q

What do Igs have secretory component?

A

IgA and IgM nly in secretions :)

64
Q

How big is IgD and what is its structure?

A

180kD, it is a monomer with 2 binding sites

65
Q

What is the serum concentration of IgD?

A

less than 30 microg/ml

66
Q

Where do you find IgD?

A

on virgin B cells that have never seen an antigen

67
Q

What is the structure of IgE, concentration and half life?

A

180 kD, monomeric with 2 binding sites, less than 100 nanograms (super small amounts). half life of 1-2 days (very short lived)
used for allergic reactions

68
Q

resting mast cells are full of granules and proteases, kinases, and tryptases and lots of specificities of IgEs. How do you get the mast cell to become activated and release its granules?

A

by having a multivalent antigen that is cross linked bind to the IgE antibody (has to close together)

69
Q

What are 2 ways to diagnosis IgE allergic responses?

A

via in vivo skin tests ([prick-puncture) and intradermal
AND
In vitro IgE tests of serum

70
Q

What are the 2 in vitro IgE tests of serum?

A

ImmunoCAP
Immunolite
HY Tec

71
Q

What are the 5 mechanisms of protection by antibodies?

A
  • neutralize toxins (tetanus, diptheria, snake)
  • Block adhesion to prevent bacterial and viral entry into cells
  • initiate complement (to opsonize bacteria and yeast)
  • Support neutrophils’ killing of yeast and bacteria
  • ADCC of infected host cells and parasites
72
Q

(blank) can block the binding chain of dimeric toxins (diptheria, tetanus)

A

antibodies

73
Q

Toxins are effective at 10 to the negative 9 M so what does this mean for antibodies?

A

they must have an affinity higher than this to be effective

74
Q

Amounts of antibody must be high enough to reach sites of infection.

A

FACT

75
Q

(blank) block bacterial adhesion to prevent bacterial entry into cells and to prevent bacterial and viral pathogens from crossing into the body from the gut

A

Antibodies

76
Q

Antibodies can initiate (blank) to opsonize bacteria and yeast.

A

complement

77
Q

C3b, iC3b, C3dg and C3d are (blank) attached (through special thioester of C3), to tag yeast or bacteria for opsonization

A

covalently

78
Q

Usually, complement (blank) products are coupled to pathogens

A

C3

79
Q

How does ADCC of infected host cels work?

A

targe cell has membrane antigen (cannot be yeast or bacteria)-> antibody is specific for that antigen-> NK cell kills the target cell

80
Q

What antibodies support ADCC?

A

IgG1 and IgG3

81
Q

How do you measure if your ADCC is working

A

You radio label with chromium 51 (which enters cells and radiolabels them) you wash the cell and only intact cels have the radiolabel. The NK cell should recognize the bound antibodies of the infected cell and then should lyse the cell which will spill radioactive into the supernate and you can measure that to make sure that your cells are getting killed properly.

82
Q

For an ADCC assay
What is this:
the counts per min (cpm) released by targets alone, without killer cells and without antibody.

A

spontaneous release (SR)

83
Q

For an ADCC assay
What is this:
the counts per min (cpm) released by targets with detergent

A

Maximum release

84
Q

For an ADCC assay
What is this:
the counts per min (cpm) released by targets with killer cells and/or with antibody

A

experimental release

85
Q

For an ADCC assay

WHat does a plus sign mean when dealing with an assay? a negative sign?

A

something was added

something was taken away

86
Q

How does Rho gam work?

A

it is an antibody feedback inhibition medicine that will block B cell signaling and make the anti-RHD B cells unresponsive so an RhD negative mommy can not attack her RhD positive baby :)

87
Q

What does neutrophil mediating killing require?

A

oxidative and nonoxidative steps

88
Q

What is the oxidative step in neutrophil mediated killing? Why is this important?

A

oxidative inchreases pH, and potassium enteres the phagosome.
It increases the potentcy of the nonoxidative step (the oxidative step would probably mediate no damage by itself)

89
Q

WHat is the nonoxidative step in neutrophil mediated killing?

A

toxic proteins from primary granules enter phagolysosomes

p91 an p21

90
Q

Neutrophil klling involves superoxide anion in the phagosome (before/after) formation of the oxidative enzyme complex. This is step 1

A

after

91
Q

How does a neutrophil assemble the oxidative enzyme compled?

A

via cytochrome p558 oxidase

92
Q

In chronic granulomatous disease (CGD) what is disrupted ?

A

step one (the oxidative step) of neutrophil killing

93
Q

(blank) is activated by neutrophil receptors to assemble the oxidase complex

A

Rac2

94
Q

Neutrophil nonoxidative step 2, proteins are added to kill the bacteria. These toxic proteins come from primary granules (modified lysosomes). The toxic proteins of the primary granules include…..?

A 
defensins
bactericidal permeability increasing factor (BPI)
phosphoplipase A
Cathepsin G,
elastase
95
Q

What is this:

4000 m.wt.; 30% of granule protein; pI = 10; poison ion pumps of bacteria

A

defensin

96
Q

What is this:

kills gram negative bacteria in seconds

A

BPI

97
Q

What is this:

generates lysolecithin, a detergent that solubilizes microbial membranes

A

phospholipase A

98
Q

Where does the oxidative burst occur and why is it needed?

A

in the phagosome to raise salt and pH so non-oxidative killing can happen

99
Q

Pyogenic bacteria and yest require (Blank) to be killed

A

oxidative step

100
Q

Patients with hereditary Chronic Granulomatous Disease (CGD) lack
the (blank) pathway and usually die from bacterial infections.

A

oxidative

101
Q

(blank) p’ts lack nonoxidative killing, have large granules in neutrophils, NK cells & hair

A

Chediak Higashi Syndrome

…sady this means their neutrophils will not kill bacteria

102
Q

What disease is this:
The mutation alters both lysosomal loading with proteins and lysosomal trafficking. The disease has neurological defects, too, which persist even after stem cell transplantation.

A

Chediak Higashi Syndrome

Block 6 Week 1 (13 decks)

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