The Immune System, 4th Edition
The Immune System, 4th Edition
4th Edition
ISBN: 9780815344667
Author: Peter Parham
Publisher: W. W. Norton & Company
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Chapter 12, Problem 15Q
Summary Introduction

(A)

To write:

Describe the ligand for the NK-cell receptor CD94: NKG2A.

Introduction:

The activation of NK cells is conducted by the expression of different activating as well as, inhibitory receptors in a manner, which prevents the NK cells from attacking the normal cells. CD94: NKG2A complex develops inhibitory signals due to the presence of immunoreceptor tyrosine-based inhibitory motives (ITIM) in the cytoplasmic tail of NKG2A, enable recruitment of tyrosine phosphatase SHP-1, SHP-2, or SHIP that inactivate signaling cascade of NK-cell activation.

Summary Introduction

(B)

To write:

The concentration of this ligand on the target cell an effective measure of the presence or absence of classical MHC class I molecules.

Introduction:

The activation of NK cells is conducted by the expression of different activating as well as, inhibitory receptors in a manner, which prevents the NK cells from attacking the normal cells. CD94: NKG2A complex develops inhibitory signals due to the presence of immunoreceptor tyrosine-based inhibitory motives (ITIM) in the cytoplasmic tail of NKG2A, enable recruitment of tyrosine phosphatase SHP-1, SHP-2, or SHIP that inactivate signaling cascade of NK-cell activation.

Summary Introduction

(C)

To write:

The Reason, this ligand considered a broad mechanism for the NK-cell detection of unhealthy cells that is relatively insensitive to MHC class I polymorphisms.

Introduction:

The activation of NK cells is conducted by the expression of different activating as well as, inhibitory receptors in a manner, which prevents the NK cells from attacking the normal cells. CD94: NKG2A complex develops inhibitory signals due to the presence of immunoreceptor tyrosine-based inhibitory motives (ITIM) in the cytoplasmic tail of NKG2A, enable recruitment of tyrosine phosphatase SHP-1, SHP-2, or SHIP that inactivate signaling cascade of NK-cell activation.

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