Studies of KIR2DL4 and HLA-G

Michael Eric Lewis Le Page

Studies of KIR2DL4 and HLA-G

Michael Eric Lewis Le Page

Research output: Thesis › Doctoral Thesis

366 Downloads (Pure)

Abstract

The thesis studied an immune system receptor called KIR2DL4, which resides on the surface of natural killer cells. KIR2DL4 was widely believed to interact with another molecule, HLA-G, and this interaction was thought critical to the acceptance of transplanted organs, for allowing a mother's immune system to accept a newly fertilized embryo, and in damping down otherwise harmful autoimmune responses. However, the results of this thesis overturned this idea by demonstrating that HLA-G and KIR2DL4 do NOT interact with each other. This finding sets a foundation for future studies aiming to find the true binding partner of KIR2DL4.

Original language	English
Qualification	Doctor of Philosophy
Awarding Institution	The University of Western Australia
Supervisors/Advisors	Witt, Campbell, Supervisor Christiansen, Frank, Supervisor Allcock, Richard, Supervisor
Award date	23 Mar 2017
Publication status	Unpublished - 2016

Access to Document

THESIS - DOCTOR OF PHILOSOPHY - LE PAGE Michael Eric Lewis - 2016
This work is protected by Copyright. You may print or download ONE copy of this document for the purpose of your own non-commercial research or study. Any other use requires permission from the copyright owner. The Copyright Act requires you to attribute any copyright works you quote or paraphrase.

Cite this

@phdthesis{6feed913181d422fb58082991bc27ebe,

title = "Studies of KIR2DL4 and HLA-G",

abstract = "The thesis studied an immune system receptor called KIR2DL4, which resides on the surface of natural killer cells. KIR2DL4 was widely believed to interact with another molecule, HLA-G, and this interaction was thought critical to the acceptance of transplanted organs, for allowing a mother's immune system to accept a newly fertilized embryo, and in damping down otherwise harmful autoimmune responses. However, the results of this thesis overturned this idea by demonstrating that HLA-G and KIR2DL4 do NOT interact with each other. This finding sets a foundation for future studies aiming to find the true binding partner of KIR2DL4.",

keywords = "Natural killer , KIR2DL4, KIR complex, HLA-G, HLA MHC complex, Immunology, Tolerance",

author = "{Le Page}, {Michael Eric Lewis}",

year = "2016",

language = "English",

school = "The University of Western Australia",

}

TY - BOOK

T1 - Studies of KIR2DL4 and HLA-G

AU - Le Page, Michael Eric Lewis

PY - 2016

Y1 - 2016

N2 - The thesis studied an immune system receptor called KIR2DL4, which resides on the surface of natural killer cells. KIR2DL4 was widely believed to interact with another molecule, HLA-G, and this interaction was thought critical to the acceptance of transplanted organs, for allowing a mother's immune system to accept a newly fertilized embryo, and in damping down otherwise harmful autoimmune responses. However, the results of this thesis overturned this idea by demonstrating that HLA-G and KIR2DL4 do NOT interact with each other. This finding sets a foundation for future studies aiming to find the true binding partner of KIR2DL4.

AB - The thesis studied an immune system receptor called KIR2DL4, which resides on the surface of natural killer cells. KIR2DL4 was widely believed to interact with another molecule, HLA-G, and this interaction was thought critical to the acceptance of transplanted organs, for allowing a mother's immune system to accept a newly fertilized embryo, and in damping down otherwise harmful autoimmune responses. However, the results of this thesis overturned this idea by demonstrating that HLA-G and KIR2DL4 do NOT interact with each other. This finding sets a foundation for future studies aiming to find the true binding partner of KIR2DL4.

KW - Natural killer

KW - KIR2DL4

KW - KIR complex

KW - HLA-G

KW - HLA MHC complex

KW - Immunology

KW - Tolerance

M3 - Doctoral Thesis

ER -

Studies of KIR2DL4 and HLA-G

Abstract

Access to Document

Fingerprint

Cite this