Exam #3 Flashcards

1
Q

Vladimir Badovinac & John Harty

A

Death of effector T cells is independant of clearance of infection

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2
Q

Sue Kaech & Rafi Ahmed

A

Memory Cells are present during effector phase of T cell response and can be definied by expression of IL–7R chain

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3
Q

Joe Sun & Mike Bevan

A

CD8 T cells that are primed without CD4 T cells don’t have memory. Possible mechanism is that these cells have proliferated more and have then died?

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4
Q

Th1 Cells

A

Intracellular pathogens, Macrophages,
cytokines affecting differentiation IL-12 & IFN-g,
STAT pathway is STAT1 (IL-12) and STAT4 (IFN-g),
Transcription factor is T-bet,
Cytokines produced by CD4 helper cell: IFN-g
B cell isotypes induced: IgGa, IgG3
Beneficial effects: Macrophage activation, clearence of intracellular pathogens
Harmful effects: Systemic pathology

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5
Q

Th2 Cells

A
Extracellular parasites
Eosinophils, basophils, mast cells
Cytokines affecting differentiation: IL-4
STAT pathwy: STAT6
Transcription factor: GATA3
Cytokines produced: IL-4, IL-5, IL-13,
B cell isotypes induced: IgE, IgG1
Beneficial effects: Eosinophil, basophil, and mast cell activation, clearence of extracellular pathogens,
Harmful effects: Allergies and asthma
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6
Q

Th17

A

Extracellular bacteria/fungi
Neutrophils
Cytokines affecting differentiation: IL-6, IL-23
STAT pathway: STAT3
Transcription factor RORgt
Cytokines produced: IL-17, IL-6
B cell isotypes induced: IgA, IgG2b
Benefits: Neutrophil activation, clearence of extracellular bacteria/fungi
Harful effects: Autoimmunity and Inflamation

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7
Q

Treg

A
Activated by ongoing immune response
Cytokines affecting differentiaion: IL-2
STAT pathway +: STAT5
Transcription factor: FOXP3
Cytokines produced: IL-10, TGF-b
Does not induce B cell isotypes
Inhibits overaction of other T cells
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8
Q

What are the 3 ways AID induced mutation can be repaired?

A
  1. Replication –> GC pair and AT pair
  2. Repair using MSH2/6 –> GC and mutates nearby AT segments
  3. Cleavage by UNG to abasic site and repair of abasic site by REV1 –> Cleave U and replaces with a random base
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9
Q

IFNy

A

Produced in response to systemic infection, signals through STAT1, induces Igy S-transcripts and IgG. Results in systemic antibodies

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10
Q

TGFb

A

Produced in response to T cells in mucosal lymphoid tissue, signals through smad 2/3, induces Iga S-transcripts and IgA. Results in mucosal antibodies

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11
Q

IL-4

A

Produced in response to pathogens at epithelial surface, signals through STAT3/6, Induces Ige S transcripts IgE, Allows mast cells to enhance immunity at epithelial surfaces

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12
Q

Name 4 routes for antigen to be taken up for presentation to T cells

A
  1. receptor mediated phagocytosis (LN resident DC)
  2. macro-pinocytosis (LN resident DC)
  3. viral infection (any DC)
  4. Cross presentation after phagocytic or macropinocytic uptake (dv103+ DC)
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13
Q

CD103+ DC

A

Migratory DC that is good at Ag cross-presenting and starting a T cell response

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14
Q

Plasmacytoid

A

LN Resident DC that is the main source of Type I IFN

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15
Q

IgM

A

antibody whose main function is complement activation and initial killing of microbes

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16
Q

IgG

A

Main serum antibody ( 4 subtypes) main function is neutralization, opsonization for phagocytosis, NK cell activation via Fc receptors, complement activation

17
Q

IgA

A

Main mucosal antibody (2 subtypes) Main function if neutralization in mucosa

18
Q

IgE

A

Epithelial surface antibody that binds to Fc receptors on mast cells and basophils

19
Q

FRN

A

Follicular Reticular Network in LN that free Ag ride in, T cells and DC cells travel on, ect

20
Q

Transcytosis

A

The process of going through a macrophage to another side

21
Q

AID

A

Acivation Induced Deaminase. Triggered by CD40 signalling adn converts C to U.

22
Q

CD40 signalling

A

B cells activated by agiC3b or BCR crosslinking upregulate CD40. T cells activated by DC express CD40L and migrate to B zone. Signalling gets full activation for both T and B cells.

WIthout this B cell forms primary foci for short lived IgM response

23
Q

Cross-linking

A

T cell independant. Cross-linking of BCR and CR2. Occurs due to multipble Ags and iC3b on microbial surfaces or FDC

24
Q

What are the steps for a lymphocyte to enter the LN via HEV

A

Rolling: Selectins such as L-selectin (aka CD62L)
Activation: Chemokines such as CCL21
Adhesion (makes high affinity): Integrins suchas LFA-1
Diapedesis: chemokines such as CL21 and CXL12

25
Q

L-selectin (aka CD62)

A

expressed on all naive T cells, for rolling stage of entrance to LN via HEV

26
Q

LFA-1

A

expressed on naive cells but upregulated by inflammatory cytokines to increase entry during LN inflammation caught by CCR7RExpressed by T cells to enter lymph node, then replaced by S1P1 receptor to migrate towards efferent LN
(activation increases CCR7 inatead of S1P1 receptor

27
Q

How do migratory DC enter LN?

A

Afferent lymphatics, slip and slide

28
Q

P- Selectin

A

Caught by CCR9 and goes to gut with integrin a4b7

29
Q

What are the 3 signals of T cell activation?

A

TCR -> MHC:Ag binding
Costimulatory protein binding ligand on DC
Cytokine signal (ex IL-2 (for proliferation), IL-12, TFGb) *May be replaced by strong MHC:Ag binding and Costimulatory proteins binding to ligand on DC`

30
Q

What is the purpose of TCR co-receptors?

A

They stabilizze TCR:MHC binding and bring associated protein kintase (PTK) to the TCR

31
Q

E-selectin

A

Caught by CCR4 and goes to skin. Uses LFA-1 and a4ba integrins