Immunopathology Type I Flashcards Preview

MS1 - Blood & Lymph > Immunopathology Type I > Flashcards

Flashcards in Immunopathology Type I Deck (10)
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1
Q

IgE sticks to mast cells through its _____ end.

A

Fc

2
Q

Eosinophils secrete _________, the only human-made substance that can kill helminths.

A

Major Basic Protein (MBP)

3
Q

Upon infection with worms, the immune system makes _________.

A

both IgG and IgE against the worm

4
Q

Helminths are not susceptible to __________.

A

complement-induced lysis

5
Q

What two mechanisms lead to the body fighting worm infections?

A

Mast cells (coated with IgE against the worms) binds to the IgG-coated worms and releases histamine; histamine then indues peristalsis, which helps the body excrete worms. Eosinophils similarly bind to the IgG around a worm and degranulate, but they release MBP, which kills the parasite.

6
Q

What role does Th2 play in parasite infections?

A

It finds the parasite (after circulating through the blood) and secretes IL-4 and IL-5 that attracts mast cells and eosinophils. Additionally, these lymphokines cause macrophages to switch to M2 activation, so that they can wall off pathogens.

7
Q

What attracts eosinophils?

A

ECF-A2, a complex of

8
Q

How do mast cells and IgE mediate the allergic response?

A

The basic mechanism is straightforward: IgE binds strongly to FcεR1 receptors on the surface of mast cells. When 2 adjacent IgE molecules so bound are cross-linked by allergen, the mast cell is signaled to release the contents of its characteristic granules, including histamine, which causes local or systemic vasodilation and increased permeability, and gut and bronchial smooth muscle contraction. Biochemical processes are launched as well, which lead to the late-phase reaction, see below.

9
Q

Hyper IgE syndrome results from _______.

A

inability to produce IFNgamma, resulting in high Th2 levels and thence high IgE levels

10
Q

Describe the late phase reaction.

A

In activated mast cells, arachidonic acid is cleaved by phospholipase C and initiate the prostaglandin/leukotriene pathway, leading to eventual inflammation.

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