Journal
MOLECULAR IMMUNOLOGY
Volume 46, Issue 6, Pages 1011-1019Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.molimm.2008.09.035
Keywords
NK cells; NKG2D; NKG2D ligands
Categories
Funding
- ACS [RSG-02-172-LIB]
- ROTRF [111662730]
- NIH [R01 A1064826-01, U19 A1062627-01, NO1-HHSN26600500032C]
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI064828, U19AI062627] Funding Source: NIH RePORTER
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Unlike T and B cells, NK cells lack variable, clonotypic receptors that recognize foreign antigens. Instead, NK cells depend on conserved receptors such as NKG2D. NKG2D recognizes a variety of inducible self-proteins that belong to the non-classical MHC class I family. They include ULBP (1-3), MIC (A & B) in human and H60 (a, b & c), Rae-1 (alpha-epsilon) and Mult1 in mice. These self-proteins are expressed due to pathological stimuli, share limited amino acid homology and form the molecular basis for NKG2D-mediated activation. Recent studies have vastly improved our understanding of NKG2D receptor-mediated activation, signaling and function. However, a detailed knowledge on the immunobiology of its ligands is lacking. How many is too many? Is NKG2D the only receptor for these ligands? Where are these ligands expressed? What are the molecular mechanisms that regulate their expression? Do normal cells express these ligands? Does the communication between NKG2D receptor and its ligands travel through a two way road? If so. what do the 'target' cells get in turn, only death? How efficient are these ligands as molecular targets for NK cell-mediated tumor immunotherapy? (C) 2008 Elsevier Ltd. All rights reserved.
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