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Fundamentals 1 > T-cell maturation / immuno week 6 > Flashcards

T-cell maturation / immuno week 6 Flashcards

1
Q

What is the first step of T-cell maturation when the cell reaches the thymus?

A

rearrange TCR genes (specifically beta chain)

after beta chain rearranges, you make pre-TCR

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2
Q

What does pre-TCR signal?

A

starts proliferation / double positive expression on T-cells

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3
Q

What happens after proliferation in the thymus?

A

positive selection

T-cells express both CD8 and CD4

occurs in thymic cortex

*make sure TCR recognize antigens presented by MHCs

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4
Q

What happens after positive selection?

A

negative selection at the cortex-medullary boundary (medullary more)

cells only positive for CD8 OR CD4

selects for TCR that attacks MHC + self with a low binding affinity (never receive a signal for apoptosis)

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5
Q

MHC-restricted

A

T-cells are MHC-restricted after they pass positive and negative selection

can only bind to peptide antigens in the context of the MHC molecules presented by their hosts

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6
Q

Where do T-cells go after the thymus?

A

to secondary lymphoid organs (lymph nodes + spleen)

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7
Q

Immune tolerance

A

refers to the ability of immune system to recognize a wide variety of potentially pathogenic microorganisms and react to self-structures

need to discriminate self from not-self

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8
Q

Central tolerance

A

tolerance to self antigens that is established in lymphocytes during development in primary lymphoid organs (thymus or bone marrow)

removes strongly autoreactive lymphocytes

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9
Q

Peripheral tolerance

A

tolerance to antigens encountered by mature lymphocytes in peripheral tissues

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10
Q

AIRE

A

involved in self-tolerance

transcription factor

turns on expression of self proteins in the thymus

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11
Q

APECED

A

a severe and fatal autoimmunity causes by mutations in the AIRE gene

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12
Q

What happens if an antigen binds strongly to self-cell presented by AIRE transcription factors?

A

the T-cell is deactivated

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13
Q

What happens if a T-cell binds moderately to self-antigen?

A

cells develop into regulatory T-cells (Tregs)

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14
Q

What transcription factor is essential for Treg development and function?

A

Foxp3

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15
Q

Where does B-cell central tolerance occur?

A

in the bone marrow

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16
Q

List the 4 peripheral tolerance mechanisms

A

Anergy

Activation induced cell death (AICD)

Suppression by regulatory Treg and Breg

Immune privilege

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17
Q

Anergy

A

state of non-responsiveness to antigen

peripheral tolerance mechanism

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18
Q

IPEX Syndrome

A

mutation in Fox3p gene

leads to multiple autoimmune diseases in infancy

no Tregs

19
Q

How do Tregs work?

A

they can regulate overactive T-cells

secrete anti-inflammatory cytokines that inhibit T-cells or other immune cells

20
Q

immunologically privileged sites

A

sites in the body where the immune system is dampened down

21
Q

Examples of immunologically privileged sites

A

brain, eye, testis, uterus

22
Q

3 ways immune privileged sites work”

A
  1. not surrounded by conventional lymphatics + tissue barriers
  2. use non-inflammatory Th2 responses
  3. expression of Fas ligand by tissues of privilege. induce apoptosis in Fas-bearing lymphocytes that try to enter these sites
23
Q

What do you need to develop an autoimmune disease?

A

combination of genes and environment

24
Q

Are autoantibodies always cause of disease?

A

no, sometimes they are the symptoms of a disease

25
Q

How are MHC genes involved in autoimmunity?

A

mutated MHCs will present self-peptides more

26
Q

What are the two major forms of autoimmune disease?

A

organ specific and systemic (lupus)

27
Q

Polymorphism

A

multiple genes produce autoimmunity

allelic mutations in genes that control immune activation

28
Q

What major groups of genes are implicated in autoimmunity

A

MHC

cytokine + signaling pathways

sex differences

29
Q

PTPN22

A

gene that controls immune activation

associated with rheumatoid arthritis

30
Q

What 2 mechanisms can lead to activation of self-reactive T-cells? (mechanisms that leads to autoimmunity)

A

molecular mimicry

bystander activation through APC maturation

31
Q

Examples of molecular mimicry (2)

A

M protein of GAS strep is similar to myosin and causes rheumatic heart disease

Herpes virus can resemble a corneal protein (herpes stromal keratitis) (HSV1 UL6)

32
Q

Bystander activation

A

tissue damage can lead to release of sequestered antigens

co-factors are present to activate immune response to tissues

33
Q

Example of bystander activation

A

Sympathetic opthalmia

one eye is damaged

antigens are released and travel to the lymph node where T cells activate

T cells can then travel to both eyes and cause damage

34
Q

How can antibodies be pathogenic?

A

directly kill cells

recruit innate cells to kill

activate receptor

block receptor

35
Q

IgM

A

type of antibody

complement activation

36
Q

IgG

A

most common circulating antibody in blood

neonatal immunity through placenta transfer

37
Q

IgE

A

type of antibody

allergy and inflammation

38
Q

IgA

A

type of antibody

mucosal immunity

39
Q

Autoimmune hemolytic anemia

A

antibodies by antigen on RBC

directly kill RBCs

40
Q

Graves’ disease

A

antibodies bind TSH receptors

leads to constant activate to produce thyroid hormones

41
Q

Goodpasture’s syndrome

A

antibodies recognize collage (type IV) in basement membrane

bind to basement membrane in glomerulus or alveoli

cause inflammation of alveoli and Glomerulonephritis/kidney failure

42
Q

Myasthenia gravis

A

antibodies bind to acetylcholine receptor

block ability for acetylchoine to bind

causes muscle weakness + ptosis

43
Q

Graves vs. Hashimoto

A

Graves causes hyperthyroidism by antibodies activating the TSH receptor

Hashimoto causes hypothyroidism by antibodies binding directly to follicular cells and causing cell death

Fundamentals 1 (29 decks)

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