Exam 2: Memory and Human Microbiome Flashcards

1
Q

What is the longest lived Abs? how long do they live? What does this mean to us?

A

IgG; live for a month or two

therefore, Abs must be made continuously to confer the immunity

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2
Q

What three kinds of B cells are made when B cells are activated from initial invader?

A
  1. Short-Lived Plasma Cells
  2. Long-Lived Plasma Cells (memory cells)
  3. Central Memory B Cell (memory cell)
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3
Q

Where are short-term and long-term plasma cells produced?

A

in lymphoid follicles of secondary lymphoid organs

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4
Q

Where do short-term plasma cells travel?

Where do long-term plasma cells travel?

A

short-term–> to bone marrow and spleen

long-term–> to bone marrow

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5
Q

What type of B cell produces incredible amounts of anitbodies and live only for a few days?

A

Short-lived plasma cells

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6
Q

What type of B cells continuously produce modest amount of antibodies and provide “life-long antibody protection”?

A

long-lived plasma cells

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7
Q

What type of B cell slowly proliferates and maintains a pool of themselves and replace the long-lived plasma cells which die from old age?

A

Memory B stem cells and maintain a pool of Central memory B cells

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8
Q

If an invader is encountered a second time, when cells will quickly proliferate and making more short-lived plasma B cells?

A

Memory B stem cells (Central memory B cells)

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9
Q

Overall, what do these cells do?

  1. Short-lived B cell
  2. Long-lived B cell
  3. Central Memory cell
A
  1. massive Ab production and dies after a few days
  2. modest Ab production and always active
  3. Stem cell to replace–> long-lived B cells and short-lived B cells
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10
Q

how does B cell memory relate to primary and secondary Ab responses?

A

1st time–> delayed a bit and IgM is more prominent at start

2nd time—> Ab’s made right away much more, esp. IgG

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11
Q

T cell memory is similar to B cell memory, what are the three kinds of T cells that can be made?

A
  1. Effector T cells
  2. Memory Effector T cells
  3. Central Memory T cells
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12
Q

After activation of T cells, what do they do?

A

proliferate (10,000 fold)

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13
Q

What type of activated T cell will travel to battle site and fight, and most die of apoptosis after a few days?

A

Effector T cells

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14
Q

What type of activated T cell will travel to battle site and remain there and can stay there for at least 10 years?

A

Memory Effector T cells

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15
Q

What type of activated T cell will stay in secondary lymphoid organs and bone marrow? What do they do during a subsequent attack?

A

Central Memory T cells

quickly activate and proliferate (mostly into Effector T cells) and go to the battle site

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16
Q

During subsequent infections, how come we usually don’t even know we have been infected?

A
  • more T and B cells specific to invader
  • memory B and T cells are easier to activate
  • Memory B cells are upgraded versions–> Somatic Hypermutation and Ab class has been pre-determined and better suited for invader
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17
Q

How is innate memory different than adaptive memory?

A

Innate–> born w/ in; is static; essentially all humans have SAME innate memory

Adaptive–> expandable; remembers invaders met; UNIQUE to each human

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18
Q

T/F. No two humans have the exact adaptive memory, but they do essentially have the same innate memory.

A

TRUEEE

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19
Q

What is CAR T cells and how do they work?

A

form of immunotherapy using specific altered T cells to fight Cancer
– sample patients blood and use their T cells and modify them to produce CARs on surface (chimeric antigen receptors)

20
Q

What is the microbiome?

A

collection of microbes in and on us

- on skin and line GI tract

21
Q

What percentage of us are human and what is microbial cells?

A

10% human
90% microbial

(or 1% human genes and 99% microbial genes)

22
Q

Where do we find most gut microbes?

A

in the large intestine

23
Q

How much of our fecal material is microbial stuff?

A

about 1/2

24
Q

What cell types does out gut microbiome consist of?

A
  • bacteria
  • viruses
  • fungi
  • protozoa
25
Q

How do our colonocytes (cells from the colon) get most of there energy?

A

microbes digest fiber into short chain fatty acids (SCFA) and these SCFA provide up to 80% of the energy for colonocytes

26
Q

How do we digest a long of our carbohydrates if many plant carbohydrates are “humanly” indigestible (fiber)?

A

enzymes from our microbiome degrade them providing nutrients

provide up to 10% of calories

27
Q

When it comes ti C diff Infections, what have been some well documented ways to help these individuals?

A

fecal microbiota transplant (FMT)

28
Q

Does the gut communicate with our brain?

A

yes, communication b/w grain-gut-enteric microbiota

connections b/w reduced anxiety, stress, depression

29
Q

What did germ free mice demonstrate? What reversed this?

A

germ free–> social avoidance

a fecal transplant reversed that

30
Q

The interface b/w the gut lumen and tissue is potentially inflammatory and we need to control this, what impact may the gut microbiota have on our immune system function?

A

short chain fatty acids and butyrate–> cause production of Treg cells (which help turn down immune response)

31
Q

What are foods we can eat that promote a good flora?

A

prebiotics

32
Q

What are live microorganisms that we can swallow that can benefit to the host?

A

probiotics

33
Q

Is a mix or single species better when it comes to probiotics?

A

mix

34
Q

What type of foods naturally contain good bacteria?

A

fermented foods

35
Q

What are five reasons why the microbiome is important?

A
  1. competes with pathogens
  2. produces vitamins we absorb
  3. digest indigestable foods
  4. provides energy source for intestinal cells
  5. talk to immune system to prevent over-rxn and allow symbiosis
36
Q

What are non-inflammatory macrophages and how do they help us “deal with” microbiota?

A

in lamina propria

don’t release a great deal of cytokines

deal with normal microbiota and “small attacks”

37
Q

What antibody is important for the GI tract and regulating all the microbes? How?

A

Secretory IgA–> specifically designed for mucosal surfaces

  • can bind invaders in lamina propria and escot them back into lumen
  • don’t cause inflammation (IgA isotype doesn’t bind to and activate immune cells)
38
Q

What is on guard along entire GI tract and deal with invaders quickly, reducitn inflammation?

A

Macrophages, lyphocytes, DCs, and IgA

“educated” B and T cells

39
Q

Where do DCs and lymphocytes that are activated in mesenteric lymph nodes and lamina propia tend to go?

A

they stay there

40
Q

What is the default setting in the intestinal system?

A

anti-inflammatory

41
Q

What do intestinal epithelial cells produce that promotes development of pTregs?

A

TGFbeta

42
Q

What will pTregs produce that help create an anti-inflammatory env. in the intestinal system?

A

IL-10 and TGFbeta

43
Q

What does normal microbiota produce that promotes formation of pTregs?

A

short-chain fatty acids

44
Q

What do DCs have that bind specific commensal bacteria? What do they produce?

A

TLRs

DCs produce cytokines that CALM the immune response

45
Q

What do TLR5 on DCs detect in the lumen?

A

flagella and pathogens

46
Q

DC’s produce _____ which drives ____ development.

A

IL-6

Th17

47
Q

What are DCs constantly doing in the GI tract?

A

sampling the lumen directly