CYTOTOXICITY TOWARDS NEONATAL VERSUS ADULT BB RAT PANCREATIC-ISLET CELLS

被引：4

作者：

EKBLOND, A ^{[1
]}

SCHOU, M ^{[1
]}

BUSCHARD, K ^{[1
]}

机构：

[1] KOMMUNE HOSP COPENHAGEN,BARTHOLIN INST,DK-1399 COPENHAGEN K,DENMARK

来源：

AUTOIMMUNITY | 1995年 / 20卷 / 02期

关键词：

DIABETES; NEONATAL AND ADULT BB RATS; CYTOTOXICITY; LATE MATURATION;

D O I：

10.3109/08916939509001932

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Cell-mediated autoimmunity is believed to influence the development of diabetes in BB rats. It has been suggested that the autoimmune destruction is due to lack of tolerance induction in early neonatal life caused by delayed maturation of the pancreatic beta cells. The present experiment has been initiated to investigate if there is any difference in in vitro cytotoxicity, and therefore antigenicity, to islet cells from neonatal, young and adult diabetes prone BB rats, and to establish the possible developmental difference in these rats compared to non diabetes prone Wistar Furth rats. Islets from rats of different ages were isolated, dispersed and C-51-labeled. In vitro cytotoxicity mediated by mononuclear spleen cells from newly diabetic BB rats was measured by counting gamma-ray emission from the culture supernatant after 16 h coincubation. We found that full adult-like islet cell maturation in BB rats - as evidenced by sensitivity to cytotoxicity - is not seen before the age of 8 to 21 days after birth. In contrast adult-like cytotoxicity to neonatal islets cells from Wistar Furth rats is seen already at the age of 8 days. Thus delayed islet cell maturation is a fact observed in BB rats.

引用

页码：93 / 98

页数：6

共 20 条

[1]

Scott J., The spontaneously diabetic BB rat. Sites of the defects leading to auto-immunity and diabetes mellitus. A review, Curr. Top. Microbiol-Immunol., 156, pp. 1-14, (1990)

[2]

Crisa L., Mordes J.P., Rossini A.A., Autoimmune diabetes meljitus in the BB rat, Diab. Metab. Rev., 8, pp. 4-37, (1992)

[3]

Adams T.E., Alpert S., Hanahan D., Non-tolerance and autoantibodies to a transgenic self antigen expressed in pancreatic beta cells, Nature, 325, pp. 223-228, (1987)

[4]

Buschard K., Jorgensen M., Aaen K., Bock T., Josefsen K., Prevention of diabetes mellitus in BB rats by neonatal stimulation of beta cells, Lancet, 335, pp. 134-135, (1990)

[5]

Bock T., Kjaer T.W., Jorgensen M., Josefsen K., Rygaard J., Buschard K., Reduction of diabetes incidence in NOD mice by neonatal glucose treatment, APMIS, 99, pp. 989-992, (1991)

[6]

Hansen A.K., Dagnaes-Hansen F., An introduction to the use of rodent models in diabetes research., (1990)

[7]

Aacn K., Rygaard J., Josefsen K., Petersen H., Brogren C.H., Horn T., Buschard K., Dependence of antigen expression on functional state of beta-cells, Diabetes, 39, pp. 697-701, (1990)

[8]

Sutton R., Peters M., McShane P., Gray D.W.R., Morris P.J., Isolation of rat pancreatic islets by ductal injection of collagenase, Transplant, 42, pp. 689-691, (1986)

[9]

Josefsen K., Hansen W.A., Kjaer T., Jorgensen M., Horn T., Berggren P.-O., Porsman P., Buschard K., Optimizing fluorescence activated cell sorting (FACS) of pancreatic endocrine cells, Diabetes, 39, (1990)

[10]

Nakamura N., Woda B.A., Tafuri A., Greiner D.L., Reynolds C.W., Ortaldo J., Et al., Intrinsic cytotoxicity of natural killer cells to pancreatic islets in vitro, Diabetes, 39, pp. 836-843, (1990)

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