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Immunology > Immune Regulation and Autoimmunity > Flashcards

Immune Regulation and Autoimmunity Flashcards

1
Q

Decreased expression of ___renders immune effector cells more susceptible to apoptosis in the absence of survival signals

A

anti-apoptotic Bcl-2

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2
Q

What is antigenic competition?

A

competing antigen can regulate the immune response to an unrelated antigen
- by cytokine crossregulation for example

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3
Q

What is at the centre of the immune regulatory process? why?

A

Antigen because humoral and cell-mediated immune responses diminish as antigen concentration decreases

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4
Q

What is the more simple role of antibody in the regulation of the immune response?

A

clearance of antigen by freely circulating antibody via the formation of immune complexes

Followed by phagocytosis

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5
Q

What is the role of secreted IgG in the regulation of the immune response?

A

inhibits continued activation of B cells by forming immune complexes that cross- link surface immunoglobulin and IgG Fc receptors on B cells

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6
Q

what is antibody feedback?

A

activation of a phosphatase that prevents further signalling through the B cells antigen receptor

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7
Q

give an example of an active regulatory mechanism for T cells?

A

CTLA-4 binding to B7 molecules deprives T cells of essential costimulatory signaling through CD28

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8
Q

What does ACID stand for? what is it important for?

A

Activation induced cell death

Important for the maintenance of T cell homeostasis

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9
Q

How does ACID work?

A

activated T cells express FASL on their surface as well as Fas

Trimerization of Fas can occur by interacting with FASL on neighbouring T cells

Leads to death by apoptosis

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10
Q

Mutant mice that lack functional Fas/FASL on T cells ..

A

had excessive numbers of T cells and spontaneously develop autoimmune disease.

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11
Q

When do Treg cells develop?

A

after persistent antigenic stimulation of T cells

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12
Q

What could be a clinical use of increased Treg activity?

A

diminish unwanted immune responses (lie autoimmunity) and promote desirable ones (like anti tumour)

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13
Q

Are Treg cells antigen specific?

A

Yes

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14
Q

What are the 4 mechanisms of Treg cell action?

A
  1. Cytokine deprivation
    - usually of IL-2
  2. release of inhibitory cytokines (IL-10 and TGFß)
  3. Inhibit APC cells by preventing them from up regulating B7 fam members
  4. cytotoxicity by secreting perforin and granzyme
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15
Q

Treg cells that interact with DCs via CTLA-4 (on T cell) and CD80-86 results in activation of a pathway leading to…

A

Induction of indoleamine-2,30dioxyenase (IDO) and decreased expression of inflammation-promoting cytokines and costimulatory molecules

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16
Q

What kinds of inflammatory cytokines and co-stimulatory molecules would be downregulated with CTLA-4/B7 interactions

A

inhibition of IL-6 and TNF alpha and downregulation of CD80/86

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17
Q

what is PGE2 an example of and what do they do? what are they secreted by?

A

PGE2 is an example of a prostaglandin secreted by macrophages

they inhibit immune responses in a non-specific manner

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18
Q

How do prostaglandins inhibit immune responses?

A

promote cAMP accumulation in T cells, which inhibits IL-2 synthesis and IL-2 receptor signaling.

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19
Q

Define: idiotope

A

Each antigenic determinant in the variable region

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20
Q

Define: idiotype

A

The sum of the individual idiotopes

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21
Q

Define: tolerance

A

active state of specific immunologic unresponsiveness exhibiting antigen specificity and memory that is induced by prior exposure to an antigen

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22
Q

What kind of lymphocytes is tolerance more easily induced in ?

A

immature ones

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23
Q

What are 4 factors that make an antigen prone to tolerance

A
  1. high doses
  2. introduced via oral or intravenous route
  3. absence of adjuvants and/or low levels of co-stimulation
  4. If the antigen is soluble
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24
Q

What is central tolerance?

A

deletion of self-reactive lymphocytes by apoptosis during their maturation in the bone marrow or thymus

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25
Q

Autoreactive T cells are eliminated in the ___ while autoreactive B cells are eliminated in the ___

A

thymus; bone marrow

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26
Q

What is peripheral tolerance?

A

inactivation of self-reactive lymphocytes in peripheral lymphoid tissues.

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27
Q

T regulatory cells (CD4+CD25+) act in ___tissues and ___ to down-regulate autoimmune responses by other T cell subsets

A

secondary lymphoid tissues; sites of inflammation

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28
Q

autoimmunity affect ___% of the population

A

5-7

29
Q

significantly more of which sex is affected by autoimmune diseases? why ?

A

more women because they tend to mount a more robust and Th1 type immune response

30
Q

What are the two broad categories that autoimmune diseases fit into?

A

organ specific and systemic

31
Q

What are the 2 examples of organ specific autoimmune diseases that we talked about?

A

Grave’s disease and insulin dependent diabetes mellitus

32
Q

What occurs during organ specific autoimmunity?

A

ymphocytes or antibodies bind to cell- membrane antigens, causing cell lysis and/or an inflammatory response, damaging the organ

33
Q

What causes Insulin-dependent diabetes mellitus?

A

Autoimmune response to insulin producing beta cells in the islets of Langerhans in the pancreas

34
Q

What attacks the beta cells?

A

activated CTLs

35
Q

What pro-inflammatory cytokines are produced in Insulin-dependent diabetes mellitus? what do they activate? what does this lead to?

A

IFN-γ, IL-1, TNF-α

activate macrophages leading to a DTH response

36
Q

What other factor can contribute to islet cell destruction?

A

autoantibodies

37
Q

What is the cause of Grave’s disease?

A

autoantibodies directed against specific receptors on thyroid cells mimic the effect of thyroid- stimulating hormone (TSH)

38
Q

What is the result of the autoantibodies binding to the thyroid cells?

A

they activate receptor-coupled adenylate cyclase and stimulate the production of thyroid hormones thyroxine and triiodothyronine

39
Q

Why is it that the overstimulation of the thyroid cannot be controlled in Grave’s disease?

A

Because autoantibody production is not regulated

40
Q

What causes rheumatoid arthritis? (ie. what two antibody classes react together)

A

autoantibodies of the IgM class (rheumatoid factor) that react with the Fc portion of self IgG
- form immune complexes

41
Q

Where do the IgM-IgG immune complexes deposit?

A

in the synovia of the joints

42
Q

what is the result of IgM-IgG immune complex deposition? what are the 3 hallmarks of this response?

A

chronic inflammatory response characterized by:

  • infiltration of the joints by granulocytes and monocytes
  • destruction of cartilage and collagen by hydrolytic enzymes
  • joint fusion
43
Q

what causes MS?

A

demyelinization of central nervous system tissue by T cells

44
Q

What is the result of CNS demyelinization?

A

progressive paralysis

45
Q

the MS lesions that are caused by the T cells resemble which kind of immune response ? what is involved?

A

A DTH reaction
- autoreactive Th1 cells specific for myelin basic protein produce cytokines that attract and activate monocytes, which do the actual damage to the myelin sheath of nerve fibers

46
Q

Are autoantibodies and CTLs involved in the MS pathology?

A

Yes

47
Q

The balance of what 2 factors is often a determining factor in development of autoimmunity?

A

Th1/Th2

48
Q

In most cases, organ specific autoimmunity is linked to autoreactive ____

A

CD4+ T cells

49
Q

Th1 cells tend to promote…

A

the development of autoimmunity

50
Q

Th2 cells tend to…

A

prevent the induction of autoimmunity and may also halt the progression of established autoimmune disease

51
Q

How are HLA specificities involved in autoimmunity?

A

Autoimmune diseases are often associated with the expression of certain HLA allelic specificities

52
Q

if you have one autoimmune disorder you tend to be at greater risk for….

A

an additional one

53
Q

preferential expression of certain _____ is also associated with autoimmune diseases

A

T cell receptor variable regions

54
Q

autoimmunity is most likely when an individual has __ and __ that can bind self peptide

A

MHC and TCRs

55
Q

Briefly, what are the 4 mechanisms accounting for T cell mediated generation of autoimmune disease?

A
  1. Release of sequestered autoantigens
  2. Molecular mimicry
  3. Inappropriate expression of class II MHC molecules
  4. Polyclonal B cell activation
56
Q

how does release of sequestered autoantigens lead to an autoimmune response?

A

T cells are exposed to antigens normally sequestered in the body and to which they were never rendered tolerant

57
Q

How does molecular mimicry lead to development of an autoimmune response?

A

tends to occur following exposure to a pathogen

those that express molecules closely resembling self antigen
- ex: heat shock antigens

can be found is both bacteria (like mycobacteria) and viruses (like measles P3)

58
Q

How does inappropriate expression of class II MHC lead to an autoimmune response

A

cells that don’t normally have class II MHC and also have co-stim molecules can present autoantigens to Th cells

59
Q

What is an example of inappropriate MHC II presentation

A

pancreatic beta cells from individuals with autoimmune diabetes express high levels of class I and class II MHC molecules

60
Q

How does IFN-γ promote development of an autoimmune reaction? when is it produced?

A

Produced following trauma or viral infection

up-regulating class II MHC expression

61
Q

What does IFN-y induce the expression of that can provide a costimulatory signal to autoreactive T helper cells reacting with self antigen- class II MHC complexes on pancreatic beta islet cells.

A

IL-1

62
Q

What occurs during polyclonal B cell activation? how does this lead to an autoimmune response?

A

LPS and EB virus are polyclonal activators of B cells
- dont require Th cells

Self reactive B cells that are activated in this manner can synthesize autoantibodies that contribute to autoimmune disease

63
Q

After the 4 ways of autoimmune induction, what are the 3 ways the tissue damage occurs?

A
  1. Th cells activate macrophages leading to inflammation and a DTH response
  2. Th cells secrete IFN-y inflaming target tissue and IL-2 which stimulates CTLs to attack tissue
  3. activate B cells to create and secrete mass amounts of autoantibodies
64
Q

What are 7 treatments for autoimmune diseases? (briefly)

A
  1. Plasmapheresis
  2. Immunosuppressive drugs
  3. Neutralizing antibodies
  4. Induced tolerance via oral administration of autoantigens
  5. Peptide blocking of T receptors recognizing self antigen/class II MHC
  6. administer monoclonal antibodies that target activated T cells
  7. targeted immunotherapy by vaccinating with autoreactive Th cells
65
Q

How does Plasmapheresis work? what disease types is it effective for?

A

removes autoantibodies and immune complexes from the plasma

temporary relief from the symptoms of autoantibody-mediated autoimmune disease

66
Q

What are 2 examples of immunosuppressive drugs? what doe they reduce the severity of?

A

cyclosporin A or FK506 can reduce the severity of T cell-mediated autoimmune diseases

67
Q

What do neutralizing antibodies target?

A

molecules involved in chronic inflammation

e.g., TNF-α and adhesion molecules

68
Q

How does administering autoantigens induce tolerance?

A

possibly by the induction of T regulatory cells that produce immunosuppressive cytokines such as transforming growth factor-ß.

69
Q

how does vaccinating with autoreactive T cells suppress autoimmunity

A

suppress the activity of the autoreactive T cells that cause autoimmune disease while sparing T cells with other antigenic specificities

Immunology (19 decks)

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