Beta cell MHC class I is a late requirement for diabetes

被引:98
作者
Hamilton-Williams, EE [1 ]
Palmer, SE [1 ]
Charlton, B [1 ]
Slattery, RM [1 ]
机构
[1] Australian Natl Univ, John Curtin Sch Med Res, Canberra, ACT 2601, Australia
关键词
T lymphocytes; nonobese diabetic; severe combined immunodeficient;
D O I
10.1073/pnas.1131954100
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Type 1 diabetes occurs as a result of an autoimmune attack on the insulin-producing beta cells. Although CD8 T cells have been implicated both early and late in this process, the requirement for direct interaction between these cells and MHC class I on the beta cells has not been demonstrated. By using nonobese diabetic mice lacking beta cell class I expression, we show that both initiation and progression of insulitis proceeds unperturbed. However, without beta cell class I expression, the vast majority of these mice do not develop hyperglycemia. These findings demonstrate that a direct interaction between CD8 T cells and beta cells is not required for initiation or early disease progression. The requirement for class I on beta cells is a relatively late checkpoint in the development of diabetes.
引用
收藏
页码:6688 / 6693
页数:6
相关论文
共 43 条
[1]   Perforin-independent β-cell destruction by diabetogenic CD8+ T lymphocytes in transgenic nonobese diabetic mice [J].
Amrani, A ;
Verdaguer, J ;
Anderson, B ;
Utsugi, T ;
Bou, S ;
Santamaria, P .
JOURNAL OF CLINICAL INVESTIGATION, 1999, 103 (08) :1201-1209
[2]   IL-1α, IL-1β, and IFN-γ mark β cells for Fas-dependent destruction by diabetogenic CD4+ T lymphocytes [J].
Amrani, A ;
Verdaguer, J ;
T'hiessen, S ;
Bou, S ;
Santamaria, P .
JOURNAL OF CLINICAL INVESTIGATION, 2000, 105 (04) :459-468
[3]   Checkpoints in the progression of autoimmune disease: Lessons from diabetes models [J].
Andre, I ;
Gonzalez, A ;
Wang, B ;
Katz, J ;
Benoist, C ;
Mathis, D .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1996, 93 (06) :2260-2263
[4]  
André-Schmutz I, 1999, EUR J IMMUNOL, V29, P245, DOI 10.1002/(SICI)1521-4141(199901)29:01<245::AID-IMMU245>3.3.CO
[5]  
2-F
[6]  
ASAYAMA K, 1986, J LAB CLIN MED, V107, P459
[7]   INSITU CHARACTERIZATION OF AUTOIMMUNE PHENOMENA AND EXPRESSION OF HLA MOLECULES IN THE PANCREAS IN DIABETIC INSULITIS [J].
BOTTAZZO, GF ;
DEAN, BM ;
MCNALLY, JM ;
MACKAY, EH ;
SWIFT, PGF ;
GAMBLE, DR .
NEW ENGLAND JOURNAL OF MEDICINE, 1985, 313 (06) :353-360
[8]   RECURRENCE OF INSULITIS IN THE NOD MOUSE AFTER EARLY PROLONGED ANTI-CD4 MONOCLONAL-ANTIBODY TREATMENT [J].
CHARLTON, B ;
MANDEL, TE .
AUTOIMMUNITY, 1989, 4 (1-2) :1-7
[9]   ADMINISTRATION OF SILICA PARTICLES OR ANTI-LYT2 ANTIBODY PREVENTS BETA-CELL DESTRUCTION IN NOD MICE GIVEN CYCLOPHOSPHAMIDE [J].
CHARLTON, B ;
BACELJ, A ;
MANDEL, TE .
DIABETES, 1988, 37 (07) :930-935
[10]   ADOPTIVE TRANSFER OF DIABETES INTO IMMUNODEFICIENT NOD-SCID SCID MICE - RELATIVE CONTRIBUTIONS OF CD4+ AND CD8+ T-CELLS FROM DIABETIC VERSUS PREDIABETIC NOD.NON-THY-1A DONORS [J].
CHRISTIANSON, SW ;
SHULTZ, LD ;
LEITER, EH .
DIABETES, 1993, 42 (01) :44-55