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Inflammation and Immunity > 1.4.2 T-Cell Responses to Antigens > Flashcards

1.4.2 T-Cell Responses to Antigens Flashcards

1
Q

What does Th1 CD4+ T cells release to increase activity of both macrophages and CD8+ T cells?

A

IFNgamma and TNFalpha

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2
Q

What are two of the main ways that pathogens get inside of cells?

A

1) Life cycle of pathogen requires an intracellular component (virus) 2) Phagocytosis

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3
Q

What of type of immune system mediator is unable to reach pathogens within cells?

A

Ab’s

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4
Q

What are the main types of ag’s that MHC class I respond to? Class II?

A

Class I: Intracellular Class II: Extracellular

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5
Q

For an intracellular pathogen to be recognized and presented on MHC class II, what must occur?

A

It must have an extracellular phase in which it gets phagocytosed and presented on MHC class II.

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6
Q

What is required of MHC class I to present antigen?

A

Cross-presentation, in essence, the DC phagocytoses the infected cell which contains the antigen. It then can process the antigen and present it on its MHC class I molecule.

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7
Q

What are some of the effector cells that CD4+ T cells can differentiate into?

A

Th1, Th2, Th17, or Tfh

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8
Q

Which chemokine receptor is used in homing T cells into the lymph nodes?

A

CCR7

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9
Q

What is the basic cellular processes that allow an effector T cell to leave the LN and travel to the site of infection?

A

Change expression of adhesion molecules and chemokine receptors (switch from LN homing to tissue homing)

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10
Q

What are macrophages doing at the site of infection that aids in the migration of effector cells to the site of infection?

A

Producing chemokines that attract effectors, Prod. inflammatory cytokines (IL-1 and TNFalpha) that act on endothelial cells

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11
Q

Expression of what on endothelial cells aids in the migration of effector cells to the tissue?

A

Adhesion molecules (selectins and integrins)

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12
Q

In Th1-mediated immunity, where are the effector cells? What are they and what are they working on?

A

At the site of infection; CD4+ T cells working on macrophages or CTLs working on infected MHC class I expressing cells

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13
Q

What are the two branches of Th1-mediated immunity?

A

1) CD4+ Th1 cells lead to the activation of phagocytes 2) CTLs kill cells harboring intracellular pathogens

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14
Q

What are the two ways that Th1 cells can activate macrophages?

A

Direct contact via CD40L-CD40 interactions or Cytokine IFNgamma

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15
Q

How does Th1 activation affect the function of macrophages?

A

Positive feedback; telling the macrophage to do more of the same: capture pathogen in phagolysosome, lysosomal proteases destroy pathogen, produce ROS and NO

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16
Q

When CD4+ cells engage macrophages via INFgamma and CD40L, expression of what is induced?

A

Proteases and ROS/NO-producing enzymes

17
Q

What are the three activation responses of activated macrophages?

A

Killing of phagocytosed microbe, secretion of cytokines (TNF, IL-1, chemokines, IL-12), increased expression of MHC molecules and costimulators (B7 molecules)

18
Q

What are cytokines used in the communication between macrophages and Th1 effector T cells?

A

Macrophage to Th1: IL-12 Effector Th1 to Macrophage: INFgamma

19
Q

What happens to the granules when a CTL recognizes an Ag and has conjugate formation?

A

Granules move towards the side of CTL activation (cytoplasmic rearrangement) and the CTL granules exit via exocytosis

20
Q

What are the two main types of products found within the granules? What do they do once inside the target cell?

A

Granzymes and Perforin; Perforin (as its name suggests) creates a pore on the surface of the cell, then the granzymes enter that hole and induce apoptosis

21
Q

Aside from granule release, what is another way that CTLs can induce cell death?

A

FasL (on CTL) interacting w/ Fas on the infected cell

22
Q

What types of cells use similar cytotoxicity mechanisms as CTLs?

A

NK and NKT cells

23
Q

What is the amplification loop b/t Th1 cells-macrophages?

A

Macrophages secrete IL-12 which acts on naive T cells to differentiate them into Th1 cells. Th1 cells activate macrophages to secrete more IL-12.

24
Q

What is the amplification loop b/t Th1 cells-endothelial cells?

A

Th1 cells produce TNFalpha, which acts on endothelial cells to increase adhesion molecules. Adhesion molecules recruits more T cells

25
Q

NK cells are designed to attack what type of cells? What does this prevent?

A

NK cells target cells that lack MHC class I. By attacking these types of cells, it kills pathogens that are trying to evade CTLs

26
Q

NK cells have what two types of receptors? Which is dominant?

A

Activating receptor (AR) recognizes a variety of ligands on target cells and inhibitory receptors (KIR) that recognize non-polymorphic residues on MHC class I; Inhibiting is dominant.

27
Q

What is used to present antigens to NKT cells? What is it similar to?

A

CD1; MHC class I-like molecule

28
Q

What type of antigens are recognized by NKT cells?

A

Glycolipid Ag’s

29
Q

What are four identifiable traits of NKT cells?

A

NK cell markers, TCR w/ limited variability, Specific for glycolipids + CD1, Kill via perforin/granzyme or FAS/FASL

30
Q

What branch of immunity is responsible for delayed type hypersensitivity? What pathogen is commonly associated with delayed type hypersensitivity?

A

Classic Th1 response, mycobacterium tuberculosis

31
Q

What is responsible for the 24-48 hr delay in DTH?

A

Th1 cells need to to home to site of infection, Th1 cells respond to Ag, induce detectable response

32
Q

What are 3 physical characteristics of DTH?

A

T cell/monocyte infiltration, increased vascular permeability-edma, fibrin deposition

33
Q

What is the issue with M. tuberculosis if it can be ingested by macrophages?

A

The macrophages cannot eliminate it

34
Q

Macrophage and T cell activation within the lungs in response to TB causes the formation of what? What can develop within this tissue?

A

Granulomas; caseous necrosis

35
Q

What are some of the TNFalpha blockage drugs? Why must pt’s be tested for TB before being put on these drugs?

A

Infliximab (Remicade), Adalimumab (Humira), Etanercept (Enbrel), Certolizumab (Cimzia), Golimumab (Simponi) B/c TNFalpha is important in the formation of granulomas. Granulomas help wall the body off from further damage of TB.

36
Q

What are some of the ways that pathogens have developed resistance to Th1-mediated immunity?

A

Prevent phagolysosome fusion, escape to cytoplasm, inhibit MHC class I, decoy receptors (soluble INFgamma receptors)

37
Q

What is occuring in slides a-d? (Hint: this is T cell interaction w/ target cell)

A

a) small CTL approaches target cell
b) CTL makes contact w/ target cell
c) 2 min after contact - CTL is round and granules reorientate
d) 10 min after contact - granules move into position for release

38
Q

Describe the various aspects of the image.

A

Dr. Yankee may have used/drawn this illustration 100x.

Inflammation and Immunity (51 decks)

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