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HD > 11 and 12- T cell immunity > Flashcards

11 and 12- T cell immunity Flashcards

1
Q

If an antigen is processed and presented by Class II MHC, what are the responses which may occur?

A

4 different options

Th1, Th2, Th17 or Treg

Commitment depends upon host genetics, the type of infection and which type of TLR or cytokine profile dominates in the early phase of T-cell activation.

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2
Q

Th1 function

A

Enhances and amplifies cellular mediated immunity (CMI) mainly by activating macrophage defense mechanisms and promoting cytoxic responses by CD8 lymphocytes

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3
Q

Th2 function

A

Promotes optimal antibody production

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4
Q

Th17 function

A

Promotes chronic inflammation

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5
Q

Treg function

A

Modulates or suppresses immune responses

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6
Q

T Follicular helper function

A

Promotes optimal antibody formation in germinal centers in lymph node.

Can be identified by CD278 display and upregulation of IL-6 and Il-21

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7
Q

TMMI

A

The “classic” Th1 reaction

T cell Mediated Macrophage Immunity

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8
Q

What type of cytokine leads to TMMI? Which cytokine assist with this?

A

IL-12 is the main cytokine synthesized by the DC.

IL-18 assist and amplifies IL-12 function.

Together they initiate the commitment of a Th0 (uncommitted) to a Th1 and also activate NK cells. IL-12 also serves to optimize CD8+ functions.

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9
Q

How can the Th1 cell be identified?

A

via induction of the transcription factor T-bet (aka the “master regulator”)

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10
Q

What is the critical contributing factor for TMMI propagation and maintenance?

A

Th1 cells rapidly up-regulate synthesis and display of IL-2, which serves as a vital growth factor that stimulates and supports the rapid proliferation of antigen stimulated T cells.

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11
Q

Th1 function

A

Enhances and amplifies cellular mediated immunity (CMI) mainly by activating macrophage defense mechanisms and promoting cytotoxic responses by CD8 lymphocytes.

Provides an antigen specific, efficient and rapid way for the immune system to recruit activated killer cells to the site of the infection.

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12
Q

TMMI

A

The “classic” Th1 reaction

T cell Mediated Macrophage Immunity.

Initiation and activation of TMMi usually occur in lymph node or spleen. The activated cells then migrate back to site of antigen uptake and mediate reaction.

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13
Q

What is the critical contributing factor for TMMI propagation and maintenance?

A

Th1 cells rapidly up-regulate synthesis and display of IL-2, which serves as a vital growth factor that stimulates and supports the rapid proliferation of antigen stimulated T cells.

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14
Q

IL-21

A

Also produced by the Th1 cell.

It is a potent activator of CD8 cytotoxic cells.

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15
Q

Name the “classic tetrad” of pro-inflammatory cytokines, what secretes them and their ultimate function.

A

IL-1, IL-6, IL-8 and TNF-alpha

Secreted in mass amounts by activated macrophages.

FUNCTION: Activate immune effector cells and recruit neutrophils and monocytes to sites of infection.

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16
Q

IL-1 Characteristics

A

Has wide biological effects:

(1) Works with IL-6 to elevate body temperature by its effects on the hypothalamus.
(2) Mobilize neutrophils from the bone marrow and induce marrow colony stimulating growth factors to accelerate leukocyte production.
(3) Acts on pituitary to release ACTH and adrenal corticosteroids in response to stress
(4) Facilitates T-cell responsiveness to IL-2
(5) Acts in an autocrine fashion to stimulate antigen presenting cells to be more efficient antigen presenters.

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17
Q

IL-1ra

A

A naturally occurring antagonist of IL-1. Competes for IL-1 receptors. Synthesized to prevent the destruction which would occur from an uncontrolled IL-1 response

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18
Q

IL-6 function

In what way does it differ from IL-1?

A

Redundant of IL-1 and actually works with it synergistically.

Differs from IL-1 in that it has growth and differentiation effects on B-cells and bone calcium metabolism.

19
Q

TNF-alpha

A

Has broad, but predominately pro-inflammatory effects.

Main Functions:

(1) potent M/M activator that confers the ability to kill tumor cells and microbes
(2) activates endothelium, promotes vasodilation and increased MHC expression
(3) under normal conditions, it is critical for maintaining immunologic homeostasis.

20
Q

TNF-alpha

A

Has broad, but predominately pro-inflammatory effects.

Main Functions:

(1) potent M/M activator that confers the ability to kill tumor cells and microbes
(2) activates endothelium, promotes vasodilation and increased MHC expression
(3) under normal conditions, it is critical for maintaining immunologic homeostasis.

21
Q

IL-8

A

Classified as a chemokine but functions as a cytokine.

Functions as a major (but not the sole) stimulus for proliferation, mobilization and recruitment of neutrophils to the infection site.

22
Q

Delayed Hypersensitivity (DH)

A

An archaic term for TMMI. They are one in the same.

23
Q

Suppression of NK cell Cytotoxicity

A

Suppressed by killer cell inhibitory receptors (KIR) on their surface that recognize NORMAL self-MHC markers.

In absence of self-MHC, KIR will be turned off ONLY if the target has an NK activating receptor

24
Q

Function of CD8+ T-cells

A

To DIRECTLY kill foreign, infected or mutated cells via antigen-specific cytotoxic mechanisms.

25
Q

The antigen binding CD8 cell initially requires a co-stimulatory signal. What are the main ways it can receive it?

A

(1) IFN-gamma and IL-2 secreted by neighboring NK cells.
(2) Parallel development of CD4+ cells, which produce IFN-gamma, IL-2 and IL-21.
(3) IL-21

26
Q

The 4 steps of cytotoxicity

A
  1. RECOGNITION of a cell that needs to be killed. Occurs via MHC-I presentation or NK cell reaction
  2. RAPID ADHESION. Extensive contact develops between the target and CTL (cytotoxic T-lymphocyte)/NK cell
  3. Killing steps
  4. Disengagement of the NK or CTL, thereby refreshing its killing capacity.
27
Q

Killing steps (3) for CTL/NK

A

(1) Induction of pore formation by perforin. Opens an actual physical pore into the target membrane that leads to osmotic instability.
(2) After pore formation, co-injection of granzymes (CTL serine esterases) can also kill a target cell.
(3) Apoptosis. Induced by switching on death genes via Fas/FasL signaling and activating the CASPASE system.

28
Q

What method can be used to turn off cytotoxicity? What is the result?

A

(1) Successful elimination of antigen (usually viral) eliminates infected targets

Without the presence of antigen, 90% of activated CD8 cells will die. The rest will be converted to “memory mode”.

29
Q

What cytokine is responsible for the development of Th2?

A

If the early cytokine profile is dominated by IL-4, a Th0 will become a Th2.

30
Q

How do you identify a committed Th2 cell?

A

GATA-3

31
Q

What type of antigens/pathogens promote a Th2 response and how does this differ from the type which promote a Th1 response?

A

Th2: EXTRACELLULAR. Soluble antigens circulating in blood and extracellular pathogens are the trigger.

Th1: INTRACELLULAR. Intracellular antigen or infection activates a response.

32
Q

what cells drive the conversion of Th0 to Th2?

A

Dendritic cells, other committed Th2 cells***, B cell presentation, and mast cells/basophils. All promote or produce Il-4

***the major source

33
Q

What do activated Th2 cells produce?

A

IL-21, 5, 6, and 10. These all promote B cell growth and isotype switching.

34
Q

What happens when IL-4 is in the presence of IL-21?

A
  • promotion of B cell proliferation, differentiation and survival of B cells.
  • serve as an isotype switch factor. Induces IgM- producing B-cells to synthesize IgG and IgA.
35
Q

IL-4 + IL-13 are requirements for what?

A

For an IgE response to parasites and other antigen specific IgE (allergic) responses

36
Q

IL-10

A

Produced by Th2 cells.

Strong promoter of B cell differentiation, isotype switching and proliferation. Is also a VERY POTENT SUPPRESSOR of Th1 responses.

37
Q

Th17 formation

A
  • The presence of extracellular bacteria or fungi trigger DC’s and macrophages to release tri of cytokines (TF-B, IL-6 and IL-23)
  • these lead Th0 to be driven to Th17
38
Q

Th17 function

A

Produces IL-17 which is a potent recruiter of neutrophil, especially to skin and mucosal surfaces

39
Q

Trio of initiating cytokines for Th17 response

A

IL-23 (PRIMARY), IL-6 and TGF-B

40
Q

Transcription factor for Th17

A

ROR

41
Q

Transcription factor for Treg

A

FoxP3

42
Q

Where is Treg generated?

A

(1) Thymus where the AIRE gene complex influences their auto-antigen specificity
(2) Post-thymus where, under the influence of TGF-B and IL-10, Th0 cells develop the Treg phenotype

43
Q

What is the Treg phenotype?

A

CD4+25+3+, FoxP3

44
Q

Treg is dependent on what Interleukin for survival and proliferation?

A

Il-2

HD (12 decks)

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