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MIMM 314 > Abadie lecture 2 > Flashcards

Abadie lecture 2 Flashcards

1
Q

presenting T cells in the germinal center leads to …

A

crosstalk and reciprocal activation that allows B cells to be activated and differentiate

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2
Q

what can B cells produce after their interaction with T cells

A

cytokinesssss
-proinflammatory: IL12, IL6 and TNFalpha
-regulatory cytokines like IL-10 and IL35

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3
Q

type 1 cytokines activates what type of b cells and type 2

A

type 1:Be1 cells
Type2: Be2 cells
this will also produce cytokines
same idea as th1 and th2 cells

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4
Q

B regulatory cells produce…

A

IL-10

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5
Q

B cell depletion: SLE lead to….

A

-decreased activation of CD40 cells lead to decreased autoreactive T cells
-increased expression of markers of T regs
-this restaures balance of homeostatic T cell response
-shows that B cells play a role in activation of T cells

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6
Q

true or false: Anti-CD20 does deplete plasma cells and prevents the differentiation of newly formed B cells from becoming plasma cells

A

false
Anti-CD20 does deplete not plasma cells and prevents the differentiation of newly formed B cells from becoming plasma cells

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7
Q

APC and regulation of T cell immunity; break in tolerance; B cells are not seen as….

A

b cells are not seen as primary antigen presenting cells but tend to promote the expansion of the T cell response

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8
Q

APC and regulation of T cell immunity; B and T cell feedforward loop

A

-the break in tolerance in an autoimmune disease leads to huge proliferation of both T and B cells

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9
Q

APC and regulation of T cell immunity; feedforward loop broken; what is the hypothesis

A

the hypothesis is that the removal of these cells breaks the expansion and survival of these cells

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10
Q

APC and regulation of T cell immunity; regulatory T cell expansion

A

removing B cells will lead to regulatory expansion of T cells and cytokines that will further dampen the T cell activation

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11
Q

APC and regulation of T cell immunity; tolerance re-established; regulatory feedforward loop

A

this leads of autoreactive T cells

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12
Q

Be1 cells produce

A

a th1 like response so it secretes infy and il12

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13
Q

Be2 cells produce

A

a th2 like response so it secretes il2, il13 and il2

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14
Q

what is the difference between Be1 and Be2 cells

A

Be2 cells can’t differentiate into antibody secreting cells while the Be1 cells can

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15
Q

what do B regulatory T cells produce

A

Il10 and it can dampen the activation of effector T cells

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16
Q

what can plasma cells produce

A

-antibodies
-beneficial cytokines like il10 and il35

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17
Q

which type of B cells can produce inflammatory cytokines and what are they

A

-memory b cells
-il6, gm-csf and tnf

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18
Q

true or false; plasma and memory b cells do not produce the same type of cytokines

A

true
because they don’t reside in the same tissues

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19
Q

what are the 3 compotents of humoral responses

A

-b cells
-plasma cells
-antibodies

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20
Q

in almost all autoimmune and inflammatory disease you have production….

A

-production of antibodies against self-antigens

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21
Q

true or false: in almost all autoimmune and inflammatory disease you have production of antibodies against self-antigens which are all pathogenic

A

false some of them were proved to not be

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22
Q

what can anti-cd20 do? in terms of b cell depletion therapies for ms

A

-prevents the formation of new inflammatory lesions which shows a clinical improvement and it works
-rituximab is the most popular on the market
-removing the b cells allows for the treatment to work

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23
Q

atacicept treatment; what does it do

A

-reduces circulating B cells aka plasma cells and decreases serum antibody titers

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24
Q

true or false; atacicept treatment slaps for ms and why

A

it lowkey sucks
-in the context of ms b cells produce dangerous cytokines while the plasma cells produce beneficial cytokines
-removing the b cells=the patient will improve
-removing plasma cells=patient will get worse

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25
Q

study if mouse model of ms: they observed an infiltration of mucosal plasma cells (IgA+) into the brain and the spinal cord of the animal treated with excess peptide and they observed that these cells were….. and removing these cells the animal got….

A

proinflammatory
worse

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26
Q

true or false: plasma cells have a very beneficial role in case of MS while B cells are more harmful

A

true

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27
Q

true or false: celiacs disease is an autoimmune disease

A

false
autoimmune lack inflammatory disorder due to the production of antibody against tissue (self-antigen)

28
Q

what causes celiacs disease

A

gluten induced enteropathy reversible on a gluten free diet

29
Q

what happens to some celiacs disease patients that is not a slay

A

a very small amount of these patients on a gluten free diet can become refractory and get a malignant transformation of T cells in the gut that acquire an activated phenotype with an nk receptor and develop T cell lymphoma

30
Q

celiacs disease only develops in individuals carrying….

A

-hla-dq2 or hla-dq8

31
Q

which % of the pop carries hla-dq2 or hla-dq8 mutations

A

40% but only 1% will develop the disease
-not everyone will get it because it requires the interaction of genetic, environmental and immune response factors

32
Q

which disease causes villous atrophy with intraepithelial lymphocytosis

A

celiacs disease

33
Q

where is TG2

A

in many tissues and is important in many functions

34
Q

in celiacs disease; antibodies directed to…

A

deaminated gluten peptides and tissue transglutaminase

35
Q

celiacs disease il15 in intestinal mucose

A

-overexpression of pro inflammatory cytokine
-some can have increased expression type 1 inf

36
Q

celiacs disease antigluten cd4+t cells are…. but not …

A

required but not sufficient

37
Q

celiacs disease; Gluten gives rise to…..

A

-proteins called guanidine and glutenin which are long filaments

38
Q

where do guanidine and glutenin go through

A

-the epithelial barrier where they get into contact with the transglutaminase which daemidates the gluten peptides

39
Q

guanidine and glutenin go through the epithelial barrier where they get into contact with the transglutaminase which daemidates the gluten peptides; this makes…..

A

this makes the gluten peptide have much higher affinity due to negative charge for binding to hla-dq2 and hla-dq8 on apc

40
Q

celiacts disease: apc migrates to….

A

the draining lymph node where the peptide is presented to T cells
-since this is a very pro inflammatory environment, an inflammatory T cell response will be made (Th1) and the regulatory T cells will be dampened

41
Q

in celiac disease, cd8 t cells that reside between epithelial cells are capable of….

A

becoming cytotoxic and killing epithelial cells
-they will somehow upregulate their cytotoxic components

42
Q

true or false B cells play a role in celiacs

A

yeah
-they produce antibodies against transglutaminase and gluten

43
Q

production of highly celiac disease specific antibodies that reflect that gluten is a substrate for….

A

TG2\

44
Q

in patients not being treated with gluten free diet, there’s production of…….

A

disease specific antibody compared to patients under gluten free diet
-production of antibody against deaminated form of gluten peptide which is a good indicator of disease

45
Q

how do you diagnose celiac disease?

A

through measuring the production of an antibody against transglutaminase or against deaminated gluten peptide wich mirrors the fact that TG2 has been activated

46
Q

anti-glutaminase is the golden standard and this is confirmed by…

A

biopsy

47
Q

true or false; there is a corrolation with the threshold of antibody titers associated with tissue damage in celiac

A

nah
the more severe the disease is, the more you have antibodies but there is no strict correlation

48
Q

what is plasmacytosis

A

another indication that humoral immunity might play a role is that there is a huge expansion of plasma cells in the mucosa

49
Q

in celiac; between … and …% are specific for the TF2 meaning that the plasma cell recognizes the TG2

A

1 and 10%

50
Q

true or false: 7% of plasma cells recognize gluten peptide

A

false
2%

51
Q

b cell directed therapies for the treatment of celiac disease

A

–rituximab (anti-cd20) can be used in patients that have celiac disease along with an additional autoimmune disease

52
Q

which type of cells that are required for the development of villous atrophy in a mouse model of celiac disease

A

b cells

53
Q

development of humanized model of mice that was born and raised on a gluten-free disease; this can allow to…..

A

be able to assess if B cells play a role

54
Q

development of humanized model of mice that was born and raised on a gluten-free disease; they used what type of mouse ?

A

used the mouse counterpart of the rituximab anti cd20 depleting antibody and treated the mouse with this over the course of the disease

55
Q

mouse model for celiacts disease; when does the first tissue damage will occur after starting eating gluten

A

30 days

56
Q

celiac disease; mouse model histology, what can u see

A

you can see an atrophy with the villi when the gluten is fed to the mice

57
Q

when you ko B cells in mouse model for celiac disease

A

there is a significant reduction of the atrophy in the mice suggesting that b cells are involved

58
Q

is there a tole for anti-tg2 and anti-gluten antibodies and/or immune complexes in tissue damage and systemic manifestations?

A

they don’t believe that antibodies in the context of celiac are pathogenic but they have a role
-a few studies show that they could impact the antigenesis, perturbation, intestinal permeability, attach to epithelial cells and promote leaky gut consensus

59
Q

intestinal deposits of anti-tg2 IgA and immune complexes containing gliadin specific IgA and transglutaminase in patients with celiac disease. They showed that…..

A

IgA that atises in celiac could be involved in capturing gluten peptides and transporting across the epithelium and creates an amplification of the immune response

60
Q

true or false: the repertoire of tg2-specific antibody secreting cells is not diverse and the tg2 specific antibodies have a lot of somatic mutations

A

false
the repertoire of tg2-specific antibody secreting cells is highly diverse and the tg2 specific antibodies have limited of somatic mutations

61
Q

some scientists observed that the repertoire of the tg2 specific antibody secreting cells is highly restricted with….

A

the predominant usage of vh5-51
-they also had very limited accumulation of somatic mutations

62
Q

evidence for a B cell T cell crosstalk in celiac disease; the hapten carrier model

A

-explains why we have antibody response in celiac
-complex between transglutaminase 2 and gluten peptide that will be internalized and processed leading to the production of the antibodies

63
Q

the hapten carrier model; how was it proven

A

-in vitro with a coculture of T cells in mouse cell line that expressed human tcr and cd4
-only when putting the gluten complex with B cells expecting the right hla with the T cells recognizing the right peptide they could observe T cell expansion
-indicated you need the complex between tg2 and gluten peptide to get this cross talk

64
Q

ways B cells could participate as apcs and how can that be testes

A

-fluorescent microscopy ex vivo to see when these cells come together
-cytokine production in vivo
-make a b cell line without mhc that cannit present the antigen to the t cell

65
Q

B cells are required in the case of celiacs for the acquisition of …

A

cytotoxic properties by intraepithelial lymphocytes
-main cell type impacted by the b cells are the cd8s in the epithelium
-when b cells are removed, there is a decrease in intraepithelial lymphocytes and they express less of the nk receptor, perforin and gransyme

MIMM 314 (11 decks)

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