A NOVEL FUNCTION OF ISLET-DERIVED CD8(+)T CELLS IN INITIATING AND DEVELOPING AUTOIMMUNE INSULIN-DEPENDENT DIABETES-MELLITUS IN NONOBESE DIABETIC (NOD) MICE

被引：6

作者：

AMANO, K ^{[1
]}

YOKONO, K ^{[1
]}

HASEGAWA, Y ^{[1
]}

TAKI, T ^{[1
]}

TOMINAGA, Y ^{[1
]}

YONEDA, R ^{[1
]}

NAGATA, M ^{[1
]}

KASUGA, M ^{[1
]}

机构：

[1] KOBE UNIV,SCH MED,DEPT INTERNAL MED 2,CHUO KU,KOBE,HYOGO 650,JAPAN

来源：

DIABETES RESEARCH AND CLINICAL PRACTICE | 1995年 / 28卷 / 03期

关键词：

NONOBESE DIABETIC (NOD) MICE; T CELL HYBRIDOMA; ADOPTIVE TRANSFER OF DIABETES; CD4(+)T CELLS; CD8(+)T CELLS;

D O I：

10.1016/0168-8227(95)01094-T

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Accumulated studies revealed that CD4(+)T cells were initially required for diabetes in NOD mice, whereas interaction of CD4(+)T/CD8(+)T cells is not fully understood. To address this question, we established islet-derived CD4(+)T cells and CD8(+)T cells from NOD mice. One NOD neonate that received CD4(+)T cells developed diabetes and insulitis with CD8(+)T cells. Administration of cyclophosphamide to non-diabetic recipients accelerated the development of diabetes, while none of the mice with anti-CD8 antibody did so. Similarly, it was observed that neonates that received islet-derived CD8(+)T cells developed diabetes and obvious insulitis mainly with CD4(+)T cells. Administration of anti-CD4 antibody with transfer of CD8(+)T cells inhibited insulitis. These results imply that CD8(+)T cells function as an initial element to recruit CD4(+)T cells to islets as well as a final effector.

引用

页码：161 / 172

页数：12

共 30 条

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