PMID- 16860660 OWN - NLM STAT- MEDLINE DCOM- 20060929 LR - 20201215 IS - 0065-230X (Print) IS - 0065-230X (Linking) VI - 95 DP - 2006 TI - NK cell receptors as tools in cancer immunotherapy. PG - 249-92 AB - Natural killer (NK) cells were identified 30 years ago based on their ability to "spontaneously" kill tumor cells. The basis for NK cell recognition and activation is due to a variety of receptors that bind to specific ligands on tumor cells and normal cells. Some of these receptors have the ability to inhibit NK cell function, and other receptors activate NK cell function. Therapeutic strategies for cancer therapy are being developed based on preventing NK cell inhibition or using NK cell receptors to activate NK cells or T cells. There are intriguing clinical data from studies of bone marrow transplantation that support the idea that preventing NK cell inhibition by human leukocyte antigen (HLA) class I molecules can be a means to promote graft-versus-leukemia (GvL) effects and limit graft-versus-host disease (GvHD) in acute myeloid leukemia (AML) and chronic myeloid leukemia (CML) patients. Experimental findings also support the blockade of NK cell inhibitory receptors as a way to protect against leukemia relapse. It may be possible to use our knowledge of NK cell activating receptors and their ligands to immunize patients with modified tumor cells to promote beneficial NK cell responses and development of host antitumor cytotoxic T lymphocytes (CTLs). Finally, new data support the idea of using modified NK cell receptors as a means to target patients' T cells against their own tumor cells and induce long-term immunity against them. Tumors are essentially tissues that have overcome normal regulation mechanisms, and therefore the ability to distinguish normal cells from abnormal cells is a key part of selectively attacking tumor cells. NK cells have various receptor systems designed to recognize infected and abnormal cells. Understanding NK cell receptors and their recognition mechanisms provides new tools for the development of immunotherapies against cancer. FAU - Sentman, Charles L AU - Sentman CL AD - Department of Microbiology and Immunology, Dartmouth Medical School, Lebanon, New Hampshire 03756, USA. FAU - Barber, Melissa A AU - Barber MA FAU - Barber, Amorette AU - Barber A FAU - Zhang, Tong AU - Zhang T LA - eng GR - AI07363/AI/NIAID NIH HHS/United States GR - AI51877/AI/NIAID NIH HHS/United States GR - CA101748/CA/NCI NIH HHS/United States PT - Journal Article PT - Research Support, N.I.H., Extramural PT - Review PL - United States TA - Adv Cancer Res JT - Advances in cancer research JID - 0370416 RN - 0 (Ligands) RN - 0 (Receptors, Immunologic) RN - 0 (Receptors, Natural Killer Cell) SB - IM MH - Animals MH - Humans MH - Immune System/physiology MH - Immunotherapy/*methods MH - Killer Cells, Natural/*cytology/immunology MH - Ligands MH - Major Histocompatibility Complex MH - Neoplasms/*immunology/*therapy MH - Receptors, Immunologic/biosynthesis MH - Receptors, Natural Killer Cell MH - Time Factors RF - 230 EDAT- 2006/07/25 09:00 MHDA- 2006/09/30 09:00 CRDT- 2006/07/25 09:00 PHST- 2006/07/25 09:00 [pubmed] PHST- 2006/09/30 09:00 [medline] PHST- 2006/07/25 09:00 [entrez] AID - S0065-230X(06)95007-6 [pii] AID - 10.1016/S0065-230X(06)95007-6 [doi] PST - ppublish SO - Adv Cancer Res. 2006;95:249-92. doi: 10.1016/S0065-230X(06)95007-6.