Can NK cells be a therapeutic target in human diseases? Can NK cells be a therapeutic target in human type 1 diabetes?

被引：18

作者：

Dotta, Francesco ^{[1
,2
]}

Fondelli, Cecilia ^{[1
]}

Falorni, Alberto ^{[3
]}

机构：

[1] Univ Siena, Dept Internal Med Endocrine & Metab Sci & Biochem, Diabet Unit, I-53100 Siena, Italy

[2] Toscana Life Sci, Fdn Umberto Di Mario ONLUS, Siena, Italy

[3] Univ Perugia, Dept Internal Med Endocrinol & Metab, I-06100 Perugia, Italy

来源：

EUROPEAN JOURNAL OF IMMUNOLOGY | 2008年 / 38卷 / 11期

关键词：

Immunotherapy; Islet inflammation; NK cells; Type; 1; diabetes;

D O I：

10.1002/eji.200838851

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Type 1 diabetes is caused by the autoimmune destruction of insulin-producing cells with consequent hyperglycemia and serious chronic complications. Both innate and adaptive immune responses participate in disease pathogenesis. Studies in animal models and in man have shown that NK cells are involved both in disease progression and in disease protection, thus suggesting that NK cells can represent a potential therapeutic target in type 1 diabetes, once the contribution of these cells to islet autoimmunity has been fully elucidated.

引用

页码：2961 / 2963

页数：4

共 23 条

[1] Type 1 diabetes: new perspectives on disease pathogenesis and treatment [J].

Atkinson, MA ;

Eisenbarth, GS .

LANCET, 2001, 358 (9277) :221-229

[2] NK cells promote islet allograft tolerance via a perforin-dependent mechanism [J].

Beilke, JN ;

Kuhl, NR ;

Van Kaer, L ;

Gill, RG .

NATURE MEDICINE, 2005, 11 (10) :1059-1065

[3] Coxsackie B4 virus infection of β cells and natural killer cell insulitis in recent-onset type 1 diabetic patients [J].

Dotta, Francesco ;

Censini, Stefano ;

van Halteren, Astrid G. S. ;

Marselli, Lorella ;

Masini, Matilde ;

Dionisi, Sabrina ;

Mosca, Franco ;

Boggi, Ugo ;

Muda, Andrea Onetti ;

Del Prato, Stefano ;

Elliott, John F. ;

Covacci, Antonello ;

Rappuoli, Rino ;

Roep, Bart O. ;

Marchetti, Piero .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2007, 104 (12) :5115-5120

[4] Target cell defense prevents the development of diabetes after viral infection [J].

Flodström, M ;

Maday, A ;

Balakrishna, D ;

Cleary, MM ;

Yoshimura, A ;

Sarvetnick, N .

NATURE IMMUNOLOGY, 2002, 3 (04) :373-382

[5] Two distinct MICA gene markers discriminate major autoimmune diabetes types [J].

Gambelunghe, G ;

Ghaderi, M ;

Tortoioli, C ;

Falorni, A ;

Santeusanio, F ;

Brunetti, P ;

Sanjeevi, CB ;

Falorni, A .

JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 2001, 86 (08) :3754-3760

[6]

Gambelunghe G, 2005, TRENDS IN IMMUNOLOGY RESEARCH, P17

[7] Association of MHC Class I chain-related A (MIC-A) gene polymorphism with Type I diabetes [J].

Gambelunghe, G ;

Ghaderi, M ;

Cosentino, A ;

Falorni, A ;

Brunetti, P ;

Falorni, A ;

Sanjeevi, CB .

DIABETOLOGIA, 2000, 43 (04) :507-514

[8] ALTERATIONS IN LYMPHOCYTE SUBPOPULATIONS IN TYPE-1 (INSULIN-DEPENDENT) DIABETES-MELLITUS - EXPLORATION OF POSSIBLE MECHANISMS AND RELATIONSHIPS TO AUTOIMMUNE PHENOMENA [J].

HEROLD, KC ;

HUEN, A ;

GOULD, L ;

TRAISMAN, H ;

RUBENSTEIN, AH .

DIABETOLOGIA, 1984, 27 :102-105

[9] EVIDENCE THAT THE REDUCED NUMBER OF NATURAL-KILLER CELLS IN TYPE-1 (INSULIN-DEPENDENT) DIABETES MAY BE GENETICALLY-DETERMINED [J].

HUSSAIN, MJ ;

ALVIGGI, L ;

MILLWARD, BA ;

LESLIE, RDG ;

PYKE, DA ;

VERGANI, D .

DIABETOLOGIA, 1987, 30 (12) :907-911

[10] Critical role for IFN-γ in natural killer cell-mediated protection from diabetes [J].

Lee, I-Fang ;

Qin, Huilian ;

Priatel, John J. ;

Tan, Rusung .

EUROPEAN JOURNAL OF IMMUNOLOGY, 2008, 38 (01) :82-89

← 1 2 3 →