T-cell Immunity Flashcards

(31 cards)

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
What is the CTL killing mechanism?
- 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
What is the granule exocytosis model?
Their is activation-induced re-orientation of granules to site of interaction - release of granzymse/perforin-->form pores - induces apoptosis in target cell
27
Can CTLs kill targets in succession?
Yes, after killing they can disengage to kill new target cell --re-synthesis granules
28
How does TC response get shut off?
* *Interaction w/ CTLA4-->**antagonist of CD28 turns off activation of TC - inhibitory receptor for B7 - Expressed on activated TCs
29
How does CTLA4 regulate TC activation?
BINDS with higher affinity to B7 then CD28 does - outcompetes CD28 binding to B7 - leads to anergy
30
What can occur if defect in CTLA4?
Autoimmune diseases
31
What are some additional factors in ending the TC response?
Elimination of Ag Elimination of other stimuli T reg cells - express CTLA4 Killing by immunoregulatory cells - shrinking TC pop so only memory cells remain