Document Detail


Potential role of NKG2D and its ligands in organ transplantation: new target for immunointervention.
MedLine Citation:
PMID:  19178412     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
NKG2D is one of the best characterized activating receptors on Natural Killer (NK) and CD8+ T cells. This receptor recognizes several different ligands (MICA/MICB and ULBPs) induced by cellular stress and infection. In addition to the role described in cancer surveillance, recent data highlight the importance of NKG2D and its ligands in organ transplantation. Allografts show evidence of MICA and MICB expression in both acute and chronic rejection. The presence of anti-MICA antibodies has been correlated with incidence of graft rejection. Furthermore, NKG2D-ligand engagement activates NK cells, which provides T-cell costimulation, and enhances antigen specific CTL-mediated cytotoxicity. Activated NK cells may function as a bridge between innate and adaptive immunity associated with transplantation. Activated NK cells in response to IL-15 can also trigger organ rejection through NKG2D and affect the maturation of both donor and recipient antigen presenting cells (APCs) and ultimately the T-cell allogeneic response. Regulatory T cells, which modulate T-cell responses in organ transplantation and infections, were reduced in numbers by NK cells exposed to intracellular pathogens, possibly via interaction with one NK2GD receptor. Blockage of NKG2D-NKG2D-L interactions provides a novel pathway for development of inhibitors. These studies have important clinical and therapeutic implications in solid organ transplantation.
Authors:
B Suárez-Alvarez; A López-Vázquez; J M Baltar; F Ortega; C López-Larrea
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons     Volume:  9     ISSN:  1600-6143     ISO Abbreviation:  Am. J. Transplant.     Publication Date:  2009 Feb 
Date Detail:
Created Date:  2009-01-30     Completed Date:  2009-03-26     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  100968638     Medline TA:  Am J Transplant     Country:  Denmark    
Other Details:
Languages:  eng     Pagination:  251-7     Citation Subset:  IM    
Affiliation:
Histocompatibility Unit, Department of Immunology, Hospital Universitario Central de Asturias, Oviedo, Spain.
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MeSH Terms
Descriptor/Qualifier:
Graft Rejection / immunology
Humans
Ligands
NK Cell Lectin-Like Receptor Subfamily K / physiology*
Organ Transplantation*
Receptors, Immunologic / antagonists & inhibitors
Chemical
Reg. No./Substance:
0/KLRK1 protein, human; 0/Ligands; 0/NK Cell Lectin-Like Receptor Subfamily K; 0/Receptors, Immunologic

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