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IHL Exam 2 > Tolerance and Autoimmunity (Michels) > Flashcards

Tolerance and Autoimmunity (Michels) Flashcards

1
Q

What is immunological tolerance

A

unresponsiveness to self antigens

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2
Q

When does autoimmunity occur

A

when immune system recognizes self antigens

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3
Q

Where does tolerance occur for lymphocytes

A

central lymphoid organs- negative selection T cells and R editing for B cells
peripheral tissues- T regulatory cells, anergy and apoptosis

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4
Q

Central tolerance for T cells occurs where

A

in thymus via negative selection. Double positive at this point

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5
Q

Formation of T reg is from which stage of tolerance

A

central tolerance.

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6
Q

What are the functions of Tregs

A

prevent autimmune disease
downmodulate immune response to allergens, cancer cells and pathogens
mediate transplantation tolerance

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7
Q

Role of T regs falls under which category of tolerance

A

peripheral tolerance

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8
Q

What cytokine to T regs need to survive

A

IL-2

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9
Q

What must lymphocytes express to become T regs

A

Foxp3 and CD25

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10
Q

What 2 general ways to Tregs downregulate T cells

A

Inhibit T cell activation and inhibit the effector functions

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11
Q

What type of T cells are Treg

A

CD4+

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12
Q

How do Tregs inhibit T cell activation

A

produce IL-10 and TGF-beta

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13
Q

What is another term for Peripheral T cell tolerance

A

T cell anergy

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14
Q

Two mechanisms of T cell anergy

A

signaling block- have Ab/Ag binding thru MHC but no Co-stimulation
use of CTLA-4 inhibits the R signaling

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15
Q

Why is peripheral tolerance necessary

A

central tolerance is not absolute

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16
Q

What induces co-stimulatroy signals

A

any “danger signals” like LPS

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17
Q

What targets the T cell in peripheral tolerance for apoptosis

A

either induction of pro-apoptotic proteins or engagement of death Receptors (Fas/FasL)

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18
Q

Induction of pro-apoptotic proteins for peripheral tolerance is mediated by what?

A

Ag recognition dependent and mitochondrial mediated

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19
Q

Mutation of FAS

A

autoimmune diseases

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20
Q

Differences in location of Ag for tolerogenic self antigens and immunogenic Ag

A

tolerogenic- in generative organs that induce neg selection

immunogenic- presence in blood and peripheral tissues permits concentration in secondary lymphoid organs

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21
Q

Describe costimulation effects in tolerogenic Ag and immunogenic Ag

A

tolerogenic- deficiency may lead to T cell anergy or apoptosis, development of T reg or sensitivity to their suppression effects
immunogenic-expression of costimulators promotes lymphocyte survival and activation

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22
Q

Compare Ag exposure in tolerogenic and immunogenic foreign Ag

A

tolerogenic- long lived persistence, (prolonged TCR engagement) may induce anergy
immunogenic- short exposure to microbial Ag = effective immune response

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23
Q

What are the T cell independent Ag types

A

self-polysaccarides, lipids and nucleic acids

24
Q

Describe central B cell Tolerance

A

Receptor editing of the light chains or NEgative selection

25
Q

Describe two mech of peripheral B cell tolerance

A

When B cell recognize self antigen without T cell help- there is a block put in Ag R so cell becomes anergic
When B cell partially recognizes self it is excluded from lympohoid follicles(necessary to survive) therefore undergoes apoptosis

26
Q

What does a B lymphocyte express in its most tolerance-senesitive stage

A

Immature B cell. has IgM no IgD

27
Q

Stimuli for tolerance of T cells

A 
central= high avidity recognition of self
peripheral= Ag presentation by APCs lacking co-stimulators. Or repeated stimulation by self Ag
28
Q

Stimuli for tolerance of B cells

A 
central= recognition of multivalent Ag in bone marrow
peripheral= Ag recognition without T cell help or second signals
29
Q

Where does anergy take place

A

peripheral tolerance. not central

30
Q

Effector mechanisms of autoimmunity

A

immune complexes
circulating autoAb
autoreactive T lymphocytes

31
Q

Principle factors in the development of autoimmunity

A

inheritance of genes and environmental factors

infections also play a role

32
Q

What factors hinder out understanding of autoimmune diseases

A

Self Ag not identified
heterogeneous and multifactorial
clinical manifestation can be prolonged and variable

33
Q

What disease is a great model for prolonged manifestation of autoimmunity

A

Diabetes Type I where there is autoimmune destruction of pancreatic Beta cells

34
Q

How can we predict whether a child will become diabetic type I

A

based on the amount of autoAb

35
Q

What is the phase called when there is loss of first insulin response

A

Pre-diabetes

36
Q

When does the clinical onset of diabetes begin

A

when body can’t keep up with the insulin demands

37
Q

Describe sex distribution of autoimmune conditions

A

majority females

38
Q

Non-HLA genes involved in Autoimmunity- SINGLE genes

A

AIRE
FoxP3
FAS

39
Q

what is characteristic of single gene defects of non-HLA in autoimmunity

A

numerous autoimmune conditions EARLY in life. Widespread autoimmunity

40
Q

IPEX is a mutation where

A

FOXP3 gene- deficient Tregs, increased IgE

41
Q

Disease assoc with mutation in FAS

A

Autoimmune lymphoproliferative syndrome (ALPS) defective apoptosis of self-reactive T cells and B cells in the periphery

42
Q

Why do IPEX kinds have increased IgE

A

T regs usually produce IL-10 and TGF-beta which inhibit TH2 usually. if Tregs deficient then TH2 overactive

43
Q

What other mutation presents similar to a FOXP3 mutation

A

CD25 mutation (IL-2 R on Tregs)

44
Q

What IL suppresses IgE and what inhibits its production

A

IL10 suppresses IgE production

TGF-beta inhibits IgE production

45
Q

Hypothesis of autoimmunity caused by microbes

A

Induction of costimulators on APCs

molecular mimicry

46
Q

What is the pathogenic component for Systemic Lupus erythematosus

A

T cells and the Ab

B cells are normal and present Ag to T cells

47
Q

What is the pathogenic component in Diabetes

A

T cells. B cells are normal and the Ab is diagnostically used but not a causative component for the disease

48
Q

What is the pathogenic component in Myasthenia Gravis

A

Ab only
T cells and Ab secretion by B cells is normal
Actual Ab blocks ACh R on mm cells

49
Q

What is the pathogenic component in Multiple Sclerosis

A

The TH1 cells are pathogenic

B cells are fine and Ab are present but f(x) unknown

50
Q

What is the postulated mech for T cell mediated autoimmunity

A

failure for central self tolerance and so when inflammation occurs APCS are activated and there is an influx of self-reactive T cells into tissues

51
Q

What cells are found to influx in diabetes type I

A

T cells influx to the islets

52
Q

Mechanisms of AutoAb

A

stimulating: Graves.
The Ab activates the TSH R causing increased thyroid hormone production
blocking: myasthenia gravis
The ab blocks ACh R on mm cells

53
Q

Symptoms of MS

A

urinary incontinence, blindness, ataxia, muscle weakness and paralysis of limbs

54
Q

Why are oligoclonal Ig found in the CNS of MS patients

A

the B cells have never been exposed to all of those self antigens

55
Q

Why are MS patients Tx with corticosteroids, cyclophophamide and IFN-Beta

A

suppress immune system

56
Q

If you treated a MS patient with IFN-gamma what would you expect

A

acceleration of disease because you are increasing TH1 response

57
Q

Why feed MBP to mice to prevent EAE

A

show T cells to recognize as self antigen. downregulate co stimulatory molecules resulting in anergy of T cells. “peripheral tolerance”

IHL Exam 2 (11 decks)

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