T-cell insulitis found in anti-GAD65+ diabetes with residual β-cell function -: A case report

被引:53
作者
Shimada, A
Imazu, Y
Morinaga, S
Funae, O
Kasuga, A
Atsumi, Y
Matsuoka, K
机构
[1] Keio Univ, Sch Med, Dept Internal Med, Div Endocrinol & Metab,Shinjuku Ku, Tokyo 1608582, Japan
[2] Saiseikai Cent Hosp, Dept Internal Med, Diabet Grp, Tokyo, Japan
[3] Saiseikai Cent Hosp, Dept Surg, Tokyo, Japan
[4] Saiseikai Cent Hosp, Dept Pathol, Tokyo, Japan
[5] Saiseikai Diabet Ctr Clin Res, Tokyo, Japan
关键词
D O I
10.2337/diacare.22.4.615
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
CASE HISTORY - We recently encountered a 65-year-old anti-GAD(-) diabetic woman with residual beta-cell function who was proved to have T-cell insulitis. The proportion of CD4(+) and CD8(+) cells varied among individual islets, although CD4(+) cells tended to be the predominant T-cell type in the islets examined. All of the islets examined still contained insulin, suggesting that beta-cell mass may have been preserved. DISCUSSION - It is well known that lymphocytic infiltration of pancreatic islets, a condition referred to as "insulitis," is seen in acute-onset type 1 diabetes at autopsy and in biopsy specimens. However, there have been no proven cases of insulitis in type 1 diabetes with residual beta-cell function. We believe that this is the first type 1 diabetic patient with residual beta-cell function who was proven to have T-cell insulitis. This novel evidence will contribute to the proper classification and treatment of diabetes and to a better understanding of the pathophysiology of type 1 diabetes.
引用
收藏
页码:615 / 617
页数:3
相关论文
共 22 条
[1]  
Berman MA, 1996, J IMMUNOL, V157, P4690
[2]   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
[3]  
DONIACH I, 1973, Clinical Endocrinology, V2, P233, DOI 10.1111/j.1365-2265.1973.tb00425.x
[4]   THE HISTOPATHOLOGY OF THE PANCREAS IN TYPE-1 (INSULIN-DEPENDENT) DIABETES-MELLITUS - A 25-YEAR REVIEW OF DEATHS IN PATIENTS UNDER 20 YEARS OF AGE IN THE UNITED-KINGDOM [J].
FOULIS, AK ;
LIDDLE, CN ;
FARQUHARSON, MA ;
RICHMOND, JA ;
WEIR, RS .
DIABETOLOGIA, 1986, 29 (05) :267-274
[5]  
Gavin JR, 1997, DIABETES CARE, V20, P1183
[6]   PATHOLOGIC ANATOMY OF PANCREAS IN JUVENILE DIABETES MELLITUS [J].
GEPTS, W .
DIABETES, 1965, 14 (10) :619-+
[7]   INVERSE RELATION BETWEEN HUMORAL AND CELLULAR-IMMUNITY TO GLUTAMIC-ACID DECARBOXYLASE IN SUBJECTS AT RISK OF INSULIN-DEPENDENT DIABETES [J].
HARRISON, LC ;
HONEYMAN, MC ;
DEAIZPURUA, HJ ;
SCHMIDLI, RS ;
COLMAN, PG ;
TAIT, BD ;
CRAM, DS .
LANCET, 1993, 341 (8857) :1365-1369
[8]   MONONUCLEAR CELL INFILTRATION AND ITS RELATION TO THE EXPRESSION OF MAJOR HISTOCOMPATIBILITY COMPLEX ANTIGENS AND ADHESION MOLECULES IN PANCREAS BIOPSY SPECIMENS FROM NEWLY-DIAGNOSED INSULIN-DEPENDENT DIABETES-MELLITUS PATIENTS [J].
ITOH, N ;
HANAFUSA, T ;
MIYAZAKI, A ;
MIYAGAWA, J ;
YAMAGATA, K ;
YAMAMOTO, K ;
WAGURI, M ;
IMAGAWA, A ;
TAMURA, S ;
INADA, M ;
KAWATA, S ;
TARUI, S ;
KONO, N ;
MATSUZAWA, Y .
JOURNAL OF CLINICAL INVESTIGATION, 1993, 92 (05) :2313-2322
[9]  
JUNKER K, 1977, ACTA PATH MICRO IM A, V85, P699
[10]   Systemic bias of cytokine production toward cell-mediated immune regulation in IDDM and toward humoral immunity in Graves' disease [J].
Kallmann, BA ;
Huther, M ;
Tubes, M ;
Feldkamp, J ;
Bertrams, J ;
Gries, FA ;
Lampeter, EF ;
Kolb, H .
DIABETES, 1997, 46 (02) :237-243