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Joeli lectures > Autoimmunity > Flashcards

Autoimmunity Flashcards

1
Q

Autoimmunity

A

loss of self tolerance due to combo of factors (we don’t tolerate self antigens)

genetic susceptibility
environmental triggers
inflammation (at the core of disease)

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2
Q

Genetic susceptibility

A

Defective regulatory proteins (Fas ligand + receptor)
MHC inheritance (vigorously present self peptides)
TCR and BCR inheritance (TC = increased killing of self; BC = increased antibodies against self)

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3
Q

Hypotheses for autoimmunity

A

Sequestered antigen
Defective peripheral tolerance
Molecular mimicry
Co-stimulator induction
Survival of self-reactive lymphocyte during clonal selection

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4
Q

What is at the core of autoimmune processes

A

inflammation

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5
Q

Sequestered antigen

A

self peptide that is not introduced to T or B cells during maturation so the T and B cells who respond to these antigens can’t be deleted

think about ocular and brain tissue

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6
Q

Defective peripheral tolerance

A

breakdown in the system that generally can suppress self reactive cells

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7
Q

Autoimmune diseases usually follow –

A

an infection

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8
Q

Molecular mimicry + examples

A

antigens of infectious pathogens closely resemble self peptides – T and B cells begin to recognize self peptides as foreign and attack it

Ex: rheumatic heart disease or T1DM

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9
Q

Costimulator induction

A

APC endocytoses microbes and vigorously present self peptides + have B7 costimulator which activates T cells

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10
Q

B cells need costimulation by

A

T reg or T helper cell

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11
Q

Cytotoxic T cell needs costimulation by

A

B7

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12
Q

Inflammation in autoimmunity

A

Cytokines amplify response
APCs activated
MHC 1 unregulated (located on all cells) –> increases number of self peptide targets

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13
Q

Allergy

A

exaggerated response to environmental antigens

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14
Q

Autoimmunity

A

misdirection of immune response against host’s own cells

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15
Q

Alloimmunity

A

immune response directed against beneficial foreign tissue (transplant or transfusion)

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16
Q

immune deficiency

A

insufficient response to protect host

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17
Q

Type 1 hypersensitivity

A

IgE-mediated (activates mast cells, basophils, eosinophils)

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18
Q

Type 2 hypersensitivity

A

Tissue specific (antigens against tissue)

Other than IgE

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19
Q

Type 3 hypersensitivity

A

immune complex mediated (Ag-Ab deposits)

20
Q

Type 4 hypersensitivity

A

Cell-mediated (T cells)

21
Q

Type 1 rxn: exposure to environmental antigen/allergen

A

dendritic cell –> TH cell
TH cell –> TH2 –> IL4, IL5, IL13
IL4—> cause B cells to class switch to IgE plasma cells to produce significant amount of IgE

22
Q

Type 1 rxn: immediate rxn

A

Allergen w IgE attracts mast cells and basophils
IgE Fc region binds to Fc receptor on mast cells and basophils –> degranulation + histamine release

1st exposure: relatively few receptors
subsequent exposures: greater number of receptors

23
Q

Type 1 rxn: Delayed rxn

A

TH2 cells recruited –> secrete IL5
IL5 –> bone marrow –> eosinophils released
Eosinophils are attracted to IgE opsonized allergen & release contents
Mast cell nucleus triggers synthesis of cytokines –> released hours later

24
Q

Type 1: anaphylaxis

A

prior sensitization to allergen
Mast cells armed with IgE

Mast cells are triggered systemically
Capillaries become leaky causing decreased blood volume
Smooth muscle constriction –> bronchoconstriction

25
Q

Type 2 hypersensitivity examples

A

RBC transfusion rxn
Graves disease
Myasthenia gravis
Goodpasture’s syndrome

26
Q

Difference between Type 2 and Type 3

A

Type 2: binds to cell surface antigens
Type 3: binds to soluble antigen in blood or body fluids and LATER deposits into tissue

27
Q

Is type 3 organ specific

A

NO

28
Q

Type 3 reactions can cause decreases in what?

A

complement proteins

Ex: post-streptococcal glomerulonephritis, SLE

29
Q

Examples of Type 4 hypersensitivity

A

Type 1 DM (against pancreatic beta cells)
Rheumatoid arthritis (action against type 2 collage in joints)
IBD
Multiple sclerosis - myelin sheath
Contact dermatitis (not autoimmune)

30
Q

What T cells are most implicated in Type 4

A

Cytotoxic T cells = destroy target cells directly

Th1 = released cytokines that recruit phagocytic cells –> cell death

31
Q

Carcinogen

A

capability to alter or disable DNA within a cell –> mutagenic activity

32
Q

Oncogene

A

mutated gene –> regulatory protein mutations

33
Q

Proto-oncogene

A

potential to become an oncogene through accelerated or positively regulated proliferation

growth factor or growth factor receptors

34
Q

Tumor suppressor genes (anti-oncogenes)

A

negatively regulate proliferations

P53

35
Q

Malignancy occurs when mutations in both

A

oncogenes maintain and not suppressed

36
Q

Results in abnormal cellular functions –> promote cancer

A

growth promotion of mutated cells
disabled feedback
decreased apoptosis
increased angiogenesis (increase blood supply to that area)
cell/tissue barriers breached
Altered immunity

37
Q

Metastases

A

invasion of distant tissues

38
Q

Macrophages against tumor

A

synthesize TNF –> destroy blood vessels supply growing tumor

Macrophage needs to be hyper activated to react –> might not happen until much later

39
Q

Viruses linked to cancer

A

HBV & liver
HPV & cervix
H pylori & stomach

40
Q

NK cells against tumor

A

in a state of constant inhibition but lose inhibition when MHC class 1 molecules are damaged/mutated

produce interferon

may not happen until later

41
Q

Checkpoint proteins

A

programmed death 1 (PD-1)

Cytotoxic T cell associated protein 4 (CTLA-4)

42
Q

CTLA-4

A

down regulates cytotoxic T cell response

active when on T cell membrane

43
Q

PD-1

A

protein on T cells that deactivates T cells when it binds to PD-1 ligand

down regulates cytotoxic T cell response

44
Q

Tumors can produce PD-1 ligand

A

normally, this can prevent overstimulation and autoimmune process
BUT

in cancer, inhibits TCR mediated positive signaling –> reduced proliferation and reduced T cell survival –> cancer wins

45
Q

Dual therapy cancer

A

CTLA-4 blockade: activation and proliferation of T cells; reduces Treg mediatied immunosuppression

PD-1 pathway blockade: restores activity of anti tumor T cells

46
Q

Autoimmune therapy goals

A

decrease autoimmune response; so increase CTLA-4 etc

47
Q

Cancer therapy goals

A

increase immune response so block CTLA-4 etc.

Joeli lectures (18 decks)

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