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Immunlogy > T-cell Immunity > Flashcards

T-cell Immunity Flashcards

1
Q

Kinetics to T cell response

A

Pathogen introduced, initially have NAIVE TCs that have not recognized Ag and have not become activated

  • once recognition occurs–>clonal expansion occurs
  • now have high #’s of TCs specific for Ag
  • They undergo EFFECTOR response
  • Once no longer needed they decline and only a few remain as memory cells
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2
Q

What do DC do?

A

They take up bacterial Ag in the skin and then move to enter the draining lymphatic vessel

  • here DC waits in TC area of LN–> wait fro TCs that are traveling from the lymph/blood to LN
  • TCs sample the DC for expression of Ag that it responds to
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3
Q

What causes DC to home into LN?

A

They express receptor CCR7, and LN express ligand for receptor

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4
Q

Ways DC process/present Ag

A

Multiple ways

–>can activate all effector TCs

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5
Q

Naive TCs

A

If TC doesnt encounter Ag it will leave and remain in circulation until correct Ag present

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6
Q

What controls migration of naive T-cells?

A

They express homing receptors

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7
Q

What are the requirements for ACTIVATING naive TCs?

A

Two Signals

  1. Ag recognition
  2. Co-stimulatory signal –> B7(APC)-CD28(TC)
    - ->needs to be high for TC to become activated
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8
Q

What occurs if only Ag recognition occurs?

A

Unresponsiveness or ANERGY

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9
Q

What occurs if only co-stimulation occurs?

A

No effect

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10
Q

B7

A

Expression primarily limited to APCs

Activation of APCs induces B7 expression @ high levels

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11
Q

When isn’t CD28 co-stimulation not required?

A 
gamma/delta TCs
CD8+ T cells
In presence of strong signal 1
High avidity responses
**EFFECTOR AND MEMORY TCs
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12
Q

What are the diff APCs?

A

DC (express MHC 2), MO (MHC1), and B-cells(MHC2)

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13
Q

Are all APCs equal in presenting Ag?

A

NO!
DC- activate a broad range of TCs
MO and BCs - activate effector and memory cells

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14
Q

Proliferation/Differentiation of activated naive TCs is driven by?

A

IL2

  • naive TCs express low affinity IL2R
  • activated TCs express high affinity IL2R and secrete IL2
  • binding of IL2 to high aff receptor sends signal to TC
  • signal induces TC proliferation
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15
Q

Do other cell surface (besides IL2) change after TC activation?

A

Yes

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16
Q

What directs activated TC to distinct anatomical sites?

A

Differential expression of adhesion molecules

  • receptors on TCs act as homing signals to guide TCs to diff places
  • target organ will express ligand for receptor
17
Q

What are the functional classes of effected CD4+ TCs? (5)

A

They all start out as THo–>and based on environement they will differentiate into certain ones

  • Th1
  • Th2
  • Th17
  • Tfh
  • Treg
18
Q

What is the importance of **CD40 ligand (TC)?

A

Critical to the ability of **CD4+ TCs to activate other cells

    • in order to have effector response and activate target they have to have a COGNATE INTERACTION
  • MO–>cell mediated immunity
  • BCs–>humoral immunity
19
Q

What is cognate interaction?

A

Interaction of BC with TC w/ specificity for the SAME Ag

20
Q

What controls whether CD4+ cell become Th1 or Th2?

A

Cytokine exposure after activation

21
Q

What determines the outcome of intracellular infections?

A

The balance between Th1 and Th2

-Th1 - cell mediated

22
Q

CD8+ cells are..

A

Cytotoxic TCs or CTLs

23
Q

CD8+ TCs activated?

A

Recognize Ag presented by MHC C1 and after co-stimulation they become activated and produce diff cytotoxins/cytokines

24
Q

How are **CD8+ TCs activated?

A

Activated by **CD28/B7

-may require additional help (from cytokines)

25
Q

What is the CTL killing mechanism?

A
  • Granule Exocytosis is the predominant PW (FAST)
  • ->**granzymes and perforin
  • Expression of cell surface TNF-fammily effector molecules (SLOW)
  • Secretion of soluble toxic cytokines (SLOW)
26
Q

What is the granule exocytosis model?

A

Their is activation-induced re-orientation of granules to site of interaction

  • release of granzymse/perforin–>form pores
  • induces apoptosis in target cell
27
Q

Can CTLs kill targets in succession?

A

Yes, after killing they can disengage to kill new target cell
–re-synthesis granules

28
Q

How does TC response get shut off?

A
  • *Interaction w/ CTLA4–>**antagonist of CD28 turns off activation of TC - inhibitory receptor for B7
  • Expressed on activated TCs
29
Q

How does CTLA4 regulate TC activation?

A

BINDS with higher affinity to B7 then CD28 does

  • outcompetes CD28 binding to B7
  • leads to anergy
30
Q

What can occur if defect in CTLA4?

A

Autoimmune diseases

31
Q

What are some additional factors in ending the TC response?

A

Elimination of Ag
Elimination of other stimuli
T reg cells - express CTLA4
Killing by immunoregulatory cells - shrinking TC pop so only memory cells remain

Immunlogy (15 decks)

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