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IHO Week 2 > Specific Acquired Immunity > Flashcards

Specific Acquired Immunity Flashcards

1
Q

Do we make lymphocytes to counterract an antigen we’re exposed to, or do we select a pre-made lymphocyte that will work?

A

we select one that we already made

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2
Q

What is the doubling time for lymphocytes?

A

6-12 hours (which is why we have to pre-make the lymphocytes if we want to stop infection)

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3
Q

THe second time you’re exposed to an antigen, the immune response to it is much faster. is this because we have more memory B cells, or because they’re easier to activate the second time?

A

both

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4
Q

How many days is typically required for the adaptive immune response to kick in?

A

7-10 days - because it takes time for the activated T cell to find the B cell with the same antigen specificity

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5
Q

What do T cells use for their receptor? B cells?

A

T cells have the T-cell receptor, which includes CD3 (which is why they all have it)
B cells use IgD as their receptor

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6
Q

What CDs do B cells have?

A

CD1, 19, 20, 23, 40, 79a, and 79b

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7
Q

What lymphocyte mediates cell-mediated immunity and which does humoral immunity?

A 
T = cell mediated
B = humoral
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8
Q

When T cells are activated, they travel to the area of inflammation where they are restimulated by local APCs, causing them to release lymphokines, which do what?

A

recruit and activate monocytes nad macrophages

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9
Q

What are the 5 specialized subtypes of helper T cells?

A
  1. Type 1 helper T cells: Th1
  2. Th17 helper T cells
  3. Type 2 helpter T cells
  4. Foliccular helper T cells
  5. Regulatory T cells
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10
Q

What are type 1 helper T cells specialized for?

A

They recognize antigen and make lymphokines to attract thousands of macrophages (active in bacterial infections, but is also the cause of host vs. graft)

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11
Q

What are Th17 cells specialized for?

A

similar to Th1, but much more powerful - implicated in serious forms of autoimmunity

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12
Q

What are type 2 helpter T cells specialized for?

A

they stimulate macrophage sto become alternatively activated - able to function in walling-off pathogens and promoting healing (usually after the Th1 response) - very important in parasitic immunity

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13
Q

What are the follicular helpter T cells specialized for?

A

they migrate from T cells areas of lymph nodes into the B cell follicles of the lymph node, where they help the B cells become activated to make antibodies

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14
Q

What do the regulatory T cells do?

A

they make cytokines that suppress the activation and function of the other T helper cells, thus keeping the immune response in check by acting as a brake

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15
Q

What to cytotoxic T cells do?

A

they kill any body cell they identify as bearing a forieng or abnormal antigen on its surface

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16
Q

What marker is on all the T helper cells that increases their affinity for antigen, helps them get activated and serves as a tag?

A

CD4

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17
Q

CD4 cells look for antigen presented on what MHC class? On what cells?
CD8 cells look for antigen presented on what MHC class? On what cells?

A 
CD4 = MHC class 2 on dendritic cells
CD8 = MHC class 1 on all cells (except RBCs)
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18
Q

Why would it be better for the immune system to kill an infected cell than to let the virus kill it?

A

Because if the virus kills the cell, it releases millions of virion particles that can make the infection worse

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19
Q

Through what ligand interaction does killer T cell killing occur?

A

thorugh FAS-FAS ligand interaction. T cells expressing FAS ligand will bind to FAS - a protein on the target cell

this causes induction of caspases and apoptosis

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20
Q

What toxic agents can also be secreted by killer T cells to lead to apoptosis?

A

TNF, perforin, and granzymes

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21
Q

For the selection process in the thymus, what is positive selection? Negative selection?

A 
positive - T cells must recognize MHC class 1 or 2 molecules in order to be stimulated to mature
negative - T cells that recognize self-antigens are driven to apoptosis (tolerance)
22
Q

Do B cells also need presentation on MHCs to become activated?

A

nope - they just need antigen

23
Q

What are the 5 major classes of antibodies?

A

IgG, IgM, IgA, and IgE

24
Q

What antibody is the most abundant antibody in the blood?

A

IgG

25
Q

When to adjacent IgG molecules bind an antigen, what do they activate?

A

the complement system

26
Q

IgG is the most abundant antibody where?

A

in the blood

27
Q

Why is IgG special in terms of newborns?

A

It’s the only antibody class that can pass from mom’s placenta into the baby’s blood

28
Q

WHat antibody develops first in response to infection before being replaced by IgG?

A

IgM

29
Q

Which is better at actiating complement - IgG or IgM?

A

IgM

30
Q

What antibody is inserted into B cell membranes as their antigen receptor?

A

IgD

31
Q

What antibody is the most important in mucous membranes?

A

IgA - secreted in saliva, gears, GI/GU fluids and milk

32
Q

Because IgA has to survive in a somewhat caustic environment of secretions, what does it have structureally to help it not be broken down?

A

secretory component

33
Q

What antibody is attached to mast cells in tissue?

A

IgE

34
Q

Antibodies are especially helpful against intra or extracellular pathogens?

A

extracellular

35
Q

Once a virus enters a cell, what lymphocyte will we need to use to get rid of it?

A

cytotoxic T

36
Q

How does an antigen and an epitope differ?

A

the antigen is the whole thing and the epitope is the specific part of the antigen that is recognized by the natibody

37
Q

What is another term for MHC?

A

human leukocyte antigen

38
Q

FOr the activation of T helper cells there are two necessary signals, which are…

A
  1. requires MHC presentation to the CD4 or 8 depending on the T cells
  2. B7-1 or B7-2 on the APC binds to the T cell surface protiein CD28 as a costimulator (or you get CD2 binding or ICAM binding or cytokines)
39
Q

What two cytokines are general activators of T cells?

A

IL-2 and IL-15

40
Q

What are two cytokins that are used to drive T celper cells to be Th1 cells?

A

IL-12 and IFN-gamma

41
Q

What cytokine is used to drive t helper cells to be Th2 cells?

A

IL-4

42
Q

What cytokine is used to down-regulate Th1 cells? Which cytokine is used to down-regulate both Th1 and Th2 cells?

A

IL-10

TGF-beta

43
Q

What’s mutated in x-linked agammaglobulinemia?

A

bruton’s tyrosine kinase, which is involved in mediating B cell maturation via the BCR - so you don’t get mature B cells and thus no antibodies

44
Q

What happens in transient hypogammaglobulinemia of infancy?

A

they don’t make antibodies appropriatly to vaccines

45
Q

What’s the isue in common variable immunodeficiency?

A

There is a mutation in MHC, so you have abnormal T-cell signalling of B cells

46
Q

What are the three general causes of SCID

A
  1. common gamma chain lack of IL-7 signalling - failure of cells to mature
  2. purine nucleoside phosphorylase deficiency
  3. adenosine deaminase deficiency
47
Q

Describe type 1 hypersensitivity

A

It’s IgE mediated to an environmental antigen - causes basophil and mast cell degranulation - asthma, allergies, anaphylactic shock

48
Q

Descrie type 2 hypersensitivity

A

Autoimmunity due to antibodies that react against self - hemolytic disease of the newborn, myasthenia gravis, good pasture’s syndrome, etc.

49
Q

Describe type 3 hypersensitivity

A

Making an antibody against a soluble antigen, causing immune complexes that can be too small for phagocytes to notice, so they get stuck in basement membranes of capillaries they travel thorugh. the trapped complexes then activate complement and inflammation causing tissue damage - arthritis, glomerulonephritis, pleurisy, rash

50
Q

Which is more worrisome: when the type 2 hypersensitivity trigger is internal or external?

A

internal - because you can never “stop” the stimulus

51
Q

Describe type 4 hypersensitivity

A

it’s cell-mediated hypersensitivity caused by activated CD4 T cells - contact hypersensitivities, tuberculin reaction, and granulomatous hypersensitivity (mycobacterium, crohn’s disease, etc)

IHO Week 2 (13 decks)

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