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Immunology > The Tantalizing Tale of T Cells > Flashcards

The Tantalizing Tale of T Cells Flashcards

1
Q

iNK T cells

A

separate population of alpha beta T cells that recognize glycolipids complexed in non-classical HLA molecules called CD1d, function through cytokines. develop prior to any VDJ rearrangments

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2
Q

gamma delta T cells

A

separate population of T cells with a unique receptor

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3
Q

order of recombination in alpha beta T cells

A

beta first: VDJ recombination, alpha locus second: VJ recombination

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4
Q

co-receptor molecules

A

either CD4 (class II MHC associations, function: suppress/help B cells) or CD8 (class I MHC associations - function: kill)

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5
Q

CD3 subunits

A

one gamme, one delta, two zeta: non-covalently associated with alpha-beta TCR dimer

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6
Q

the thymus

A

formed by epithelial cells, mesenchymal cells, and bone marrow derived hematopoietic cells that become thymocytes; has a few dendritic cells and macrophages but NO B CELLS; 3-d meshwork

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7
Q

3-d meshwork

A

of the thymus, lost in lymphopenic people, formed by the interaction of epithelial cells and the thymocytest

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8
Q

the TCR’s developmental fate

A

is determined by its weak interaction with a dendritic cell or epithelial cell’s peptide/MHC receptor (from alpha/beta T cell to the following, based on interaction – MHC II:CD4::MHC I:CD8::CD1d/glycolipid:NK)

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9
Q

double positive; single positive; double negative

A

both CD8 and CD4 receptors; either or; neither nor

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10
Q

Double Positive T cells

A

have both CD8 and CD4 molecules and are immature and are found in the thymus

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11
Q

Double Negative T cells

A

have neither receptor and are therefore B cells, found in lymph nodes

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12
Q

co-receptor development pattern

A

double negative to double positive to single positive

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13
Q

thymopoiesis

A

when double negative cells become double positive. require the cytokine IL-7 to do so.

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14
Q

beta chain rearrangements occur

A

in the double negative stage, unless a successful TCR beta locus (and pre-TCR) is expressed, the cell is arrested in the DN3 stage

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15
Q

alpha chain rearrangements

A

are initiated once the cell successfully leaves the DN3 stage, and re-expresses RAG1/2. during alpha locus rearrangements (VJ), the cell is double positive

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16
Q

3 life/death developmental fates of a alpha/beta expressing T cells

A
  1. death by neglect (what happens behin the scenes during positive selection) – when the T cell finds no HLA/peptide to interact with in the thymus 2. survival (positive selection) – when the T cell has a weak affinity to a self-HLA/self-peptide 3. death by negative selection – when the T has a strong affinity to a self-HLA/self-peptide
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17
Q

AIRE

A

a transcription factor that forces tissue specific antigens to be expressed in the thymus - mutations in AIRE cause autoimmunity

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18
Q

TRECs

A

T Cell Receptor Excision Circles: chromosomal DNA with deleted unused V and or D/J regions found in newly ‘generated’ T cells leaving the thymus, measured clinically to determine immunodeficiencies in newborns

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19
Q

FY720

A

immunosuppressive drug that blocks the movement of T cells into the blood via attachment to the S1P receptor (which usually binds to the high levels of S1P found in the blood

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20
Q

CD4 count

A

important for indicating an HIV infection - CD4 numbers less than 400 “are of immediate concern for opportunistic infections”

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21
Q

Spleen T vs. B cell count

A

T cells ~ 20 % (minority)

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22
Q

activation of what three parts of a T cell is necessary to generate a make it an “effector T cell”

A
  1. the TCR 2. a costimulatory molecule (CD28/ICOS) 3. cytokine receptor
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23
Q

effector T cells

A

no longer need three signals now that they are “committed memory T cells”

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24
Q

T cell and APC “velcro” is comprised of what

A

LFA-1, ICAM-1, VLA-4, CD2 (interactions occur in T cell enriched zones in the lymph node, the best APC is a dendritic cell)

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25
Q

T cells get from the thymus to secondary lymphoid organs via

A

HEVs, or high endothelial venules; interaction via T-cell expressed L selectin

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26
Q

T-cell/APC interactions

A

only requires 3-5 foreign agonist peptide/HLA complexes, forms the immunological synapse

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27
Q

T Cell receptor signal cascade

A

tyrosine phosphorylation –> increase in intracellular Ca2+ –> activation of calcineurin & transcriptional factors (NFAT, NF-kappaB) –
also the basis of the BCR/NK/Ig-receptor cell’s signaling pathways

28
Q

CD28

A

co-stimulatory molecule, responsible for signal 2; binds to B7-1/B7-2 (CD80/CD86) on APCs —> downstream: B7-1/-2 tails are tyrosine phosphorylated –> PI3K –> NF-kappaB –> translocated into nucleus = combined with signal 1, causes gene transcription and the release of cytokine IL-2

29
Q

cell surface proteins induced upon T cell activation

A

chemokine receptors, increased expression of the CD40 ligand, increased expression of SIP1, expression of high-affinity IL-2 receptor, CD25

30
Q

IL-2

A

secreted by the CD4 T-cell, growth factor that promotes T cell division, helps CD8 expand, works in a paracrine manner

31
Q

CD40L

A

up-regulated by CD4 T-cell, aids in T cell interaction with B cells and macrophages, one of the fundamental methods of B/T-cell interactions, and allows for isotype switching. mutations in CD40L do not allow for isotype switching (Hyper-IgM syndrome)

32
Q

Signal 3, T cell

A

signals 1&2 allow for T cell expansion. Signal 3 “instructs the T cell how to behave”. cytokine mediated - this cytokine is produced and secreted by the associated APC

33
Q

NK T cells

A

express a TCR receptor, secrete cytokines, but very rapidly, within minutes or hours of stimulation

34
Q

cytokine release

A

the type of pathogen determines the type of pathogen released, different pathogens stimulate different sets of cytokines, many cells release pathogens, dendritic cells are the main cells that release pathogens

35
Q

IL-12

A

Th1 cell differentiation via transcription factor t-bet

36
Q

IL-4

A

Th2 cell differentiation via transcription factor GATA3 – linked to allergy and atopy

37
Q

Th17

A

viral, fungal, bacterial infections. require IL-1, IL-6, TGF-beta. activation causes RORgammat activation —> IL-17 production

38
Q

Tregs

A

suppress the development and/or activation of potential auto-reactive T cells, regulate pathogen-induced inflammatory responses, control immune cell homeostasis, characterized by Foxp3 transcription factor expression, release IL-10 and TGF-beta, serve to maintain peripheral tolerance to self-proteins

39
Q

CD4 Treg cells

A

defined by the expression of the Foxp3 transcription factor, dependent on IL-2 for development

40
Q

Tfh

A

T follicular helper cell - concentrate in the germinal center and support B cell activation and somatic hypermutation, key role is the production of cytokines

41
Q

toxoplasma

A

common infection from the parasite T. gondii, required CD4 Th1 cells to clear

42
Q

Th1 cells

A

important for clearing intracellular bacteria, viruses, and parasites via the interferon pathway

43
Q

gamma-IFN

A

IL-12 induces Th1/CD8/NK cells to release this interferon, which primes cell populations to contain and eliminate infection

44
Q

Th2 helper cells

A

activated by signal 3 - IL-4, IL-25 –> secrete IL-4, IL-5, IL-13 near a B cell –> IL-4 causes the B cell to secrete immunoglobulins, IL-5/IL-13 cause the B cell isotype switching to IgE

45
Q

IL-5/IL-13

A

also activate macrophages and eosinophils

46
Q

IL-10

A

“suppressive” cytokine released by Tregs

47
Q

CD8 cell MO

A

release cytolytic granules (perforin, granzyme), resulting membrane perforations result n infected target cell lysis

48
Q

one of the key targets of cytokines released by macrophages

A

macrophages (in response up-regulate cell surface proteins and undergo a “respiratory burst” to generate

49
Q

reactive oxygen species

A

generated with the NADPH oxidase complex (anti bacterial products: hydrogen peroxide, nitric oxide, hydroxyl ions, hypochlorite)

50
Q

caseous granuloma

A

has neurotic tissue evident in the middle, made as a result of macrophages and Th1 cells surrounding and walling off mycobacterium tuberculosis, virtually pathognomonic for lung TB

51
Q

TNF and interferon

A

usually coordinate changes in other organ systems, toxic in large amounts

52
Q

of days it takes to generate a significant amount of CD8 cells

A

8-10 days

53
Q

cytokines

A

can act in a autocrine or paracrine manner

54
Q

the T cell undergoes

A

a number of time dependent genetic changes including up regulation of CTLA-1 and fas

54
Q

main mechanisms to decrease levels of T cells

A

reduction in IL-2, up-regulation of fas, expression of inhibitory molecules, differentiation of some activated T cells into memory cells

55
Q

CTLA-4

A

inhibits further TCR signaling (binds to B7-1 and B7-2 with higher affinity then CD28)

55
Q

PD-1

A

limits further T cell activation

56
Q

fas

A

binds to fasl and causes the cell to be killed

57
Q

memory T cells

A

have the characteristics of 1. memory 2. specificity

58
Q

CTLA-4

A

inhibits further TCR signaling (binds to B7-1 and B7-2 with higher affinity then CD28)

59
Q

PD-1

A

limits further T cell activation

60
Q

fas

A

binds to fasl and causes the cell to be killed

61
Q

memory T cells

A

have the characteristics of 1. memory 2. specificity

62
Q

ITIMs

A

class of proteins expressed on T, B, and NK cells that associate with protein tyrosine phosphatases. They de-phosphorylate from tyrosine residues and key signaling proteins in B and T cell activation. Examples are SHP-1, SHP-1, and SHIP

63
Q

IVIG

A

exogenous source of human Ig, can work by acting as a source of Igs to fight foreign infection or by competing with the host Ig and increasing the catabolism of host Ig (high doses hypothetically up-regulate an inhibitory FC receptor on macrophages and monocytes

Immunology (8 decks)

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