PD-1 and Its Ligands in Tolerance and Immunity

Annual Review of Immunology - Tập 26 Số 1 - Trang 677-704 - 2008
Mary E. Keir1, Manish J. Butte1, Gordon J. Freeman2, Arlene H. Sharpe1
1Department of Pathology, Harvard Medical School and Brigham and Women's Hospital, Boston, Massachusetts 02115-5727;
2Department of Medical Oncology, Dana Farber Cancer Institute, Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115-6013

Tóm tắt

Programmed death 1 (PD-1) and its ligands, PD-L1 and PD-L2, deliver inhibitory signals that regulate the balance between T cell activation, tolerance, and immunopathology. Immune responses to foreign and self-antigens require specific and balanced responses to clear pathogens and tumors and yet maintain tolerance. Induction and maintenance of T cell tolerance requires PD-1, and its ligand PD-L1 on nonhematopoietic cells can limit effector T cell responses and protect tissues from immune-mediated tissue damage. The PD-1:PD-L pathway also has been usurped by microorganisms and tumors to attenuate antimicrobial or tumor immunity and facilitate chronic infection and tumor survival. The identification of B7-1 as an additional binding partner for PD-L1, together with the discovery of an inhibitory bidirectional interaction between PD-L1 and B7-1, reveals new ways the B7:CD28 family regulates T cell activation and tolerance. In this review, we discuss current understanding of the immunoregulatory functions of PD-1 and its ligands and their therapeutic potential.

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Tài liệu tham khảo

10.1038/icb.1975.3

10.1016/1074-7613(95)90125-6

10.1126/science.270.5238.985

10.1002/j.1460-2075.1992.tb05481.x

10.1016/S1074-7613(00)80089-8

10.1126/science.291.5502.319

10.1038/70932

10.1084/jem.192.7.1027

10.1038/85330

10.1084/jem.193.7.839

10.1016/j.immuni.2007.05.016

10.1016/j.cellimm.2005.07.007

10.1038/nature01621

10.4049/jimmunol.177.12.8844

10.1111/j.1745-7254.2005.00086.x

10.1093/abbs/36.4.284

10.1084/jem.20021752

10.1016/S1074-7613(04)00051-2

10.1093/intimm/8.5.773

10.4049/jimmunol.173.2.945

10.1093/intimm/8.5.765

10.4049/jimmunol.176.5.2808

10.1073/pnas.0708767104

10.1084/jem.20061496

10.4049/jimmunol.169.10.5538

10.1080/713774061

10.1016/j.jneuroim.2004.06.013

10.1016/j.febslet.2005.12.093

10.1182/blood-2006-10-051482

10.1038/nm1517

10.1002/eji.200737461

10.1002/eji.200324228

10.1073/pnas.0931259100

10.1002/1521-4141(200203)32:3<634::AID-IMMU634>3.0.CO;2-9

10.1038/sj.emboj.7601146

10.1016/j.febslet.2004.07.083

10.1073/pnas.231486598

10.4049/jimmunol.170.2.711

10.1016/S1074-7613(01)00259-X

10.1002/eji.200526347

10.1128/MCB.25.21.9543-9553.2005

10.4049/jimmunol.166.9.5480

10.4049/jimmunol.173.6.3962

10.1016/S1074-7613(00)80103-X

10.1084/jem.20021466

10.4049/jimmunol.170.4.1830

10.1158/0008-5472.CAN-03-3025

10.1002/eji.200637002

10.4049/jimmunol.173.2.1360

10.1016/j.jaci.2005.04.038

10.1111/j.1365-2249.2005.02992.x

10.1002/eji.200635978

10.1172/JCI200316015

10.1073/pnas.0307252101

10.1038/nm955

10.4049/jimmunol.170.3.1257

10.1084/jem.191.5.891

10.4049/jimmunol.175.11.7372

10.4049/jimmunol.171.9.4574

10.1016/j.immuni.2005.01.015

10.1038/ni1165

10.1084/jem.20022125

10.1073/pnas.0505497102

10.1084/jem.20051776

10.1084/jem.20061577

10.1161/CIRCULATIONAHA.107.709360

10.4049/jimmunol.179.8.5064

10.1016/j.jneuroim.2007.01.012

10.1523/JNEUROSCI.4794-04.2005

10.1084/jem.20022119

10.4049/jimmunol.176.6.3480

10.1016/j.jneuroim.2006.10.006

10.1002/0470871628.ch6

10.4049/jimmunol.175.10.6265

10.1002/eji.200425109

10.1002/eji.200535332

10.1093/intimm/dxm057

10.1038/ng1020

10.1002/ana.20514

10.1038/sj.gene.6364383

Wang SC, 2007, J. Rheumatol., 34, 721

10.1016/j.molimm.2006.12.008

10.1084/jem.181.3.1145

10.4049/jimmunol.174.4.1888

10.1016/j.clim.2005.10.017

10.1084/jem.20022235

10.1016/j.febslet.2005.09.098

10.1038/nature04444

10.1128/JVI.78.11.5535-5545.2004

10.1038/nature05115

10.1038/nm1482

10.1128/JVI.80.7.3532-3540.2006

10.1128/JVI.02844-06

10.1128/JVI.01177-06

10.4049/jimmunol.178.10.6634

10.1111/j.1365-2893.2006.00746.x

10.1182/blood-2002-10-3065

10.1128/JVI.00024-07

10.1089/vim.2006.0096

10.4049/jimmunol.179.3.1979

10.1182/blood-2006-09-044826

10.4049/jimmunol.176.5.3000

10.1128/IAI.00553-07

10.1016/j.ijpara.2005.06.003

10.4049/jimmunol.173.2.1240

10.1002/eji.200535458

10.1097/01.tp.0000168432.60022.99

10.2741/2283

10.1111/j.1600-6143.2006.01260.x

10.4049/jimmunol.174.6.3408

10.4049/jimmunol.175.9.5774

10.4049/jimmunol.169.11.6546

10.4049/jimmunol.174.11.6648

10.4049/jimmunol.177.9.5928

10.4049/jimmunol.170.7.3637

10.1111/j.1600-6143.2005.00954.x

10.4049/jimmunol.179.8.5204

10.1161/01.ATV.0000145015.23656.e4

10.4049/jimmunol.171.3.1272

10.1097/01.tp.0000256293.90270.e8

10.4049/jimmunol.172.4.2530

10.1002/eji.200425197

10.1136/bjo.2006.091314

10.1038/nm0902-1039c

10.1073/pnas.0611533104

Strome SE, 2003, Cancer Res., 63, 6501

10.1002/cncr.22588

10.1158/1078-0432.CCR-04-0428

10.1007/s00262-006-0266-z

10.1158/1078-0432.CCR-06-2746

10.1073/pnas.0406351101

10.1016/j.acthis.2006.01.003

10.1084/jem.20031074

10.1097/01.pas.0000209855.28282.ce

10.1182/blood-2006-12-064360

10.1002/ijc.23042

Hirano F, 2005, Cancer Res., 65, 1089, 10.1158/0008-5472.1089.65.3

10.1073/pnas.192461099

10.1093/intimm/dxh194

10.1038/nm863

10.1172/JCI31911

10.1093/intimm/dxm091

10.4049/jimmunol.179.5.2860

10.1002/eji.200324270

10.1172/JCI31344

10.1073/pnas.0702579104

10.1016/S0165-2478(02)00088-3

10.1016/j.bbrc.2005.02.161

10.1111/j.1572-0241.2006.00948.x

10.4049/jimmunol.169.7.3581

10.4049/jimmunol.176.4.2238

10.1002/eji.200425405

10.1016/j.imlet.2007.04.001

153. Genomics Institute of the Novartis Research Foundation. Online database. GNF SymAtlas v1.2.4.http://expression.gnf.org