Autoimmune manifestations in the transforming growth factor-beta 1 knockout mouse

被引：172

作者：

Yaswen, L

Kulkarni, AB

Fredrickson, T

Mittleman, B

Schiffmann, R

Payne, S

Longenecker, G

Mozes, E

Karlsson, S

机构：

[1] NINCDS,DEV & METAB NEUROL BRANCH,UNIT MOUSE GNET & HUMAN DIS MODELS,MOLEC & MED GENET SECT,BETHESDA,MD 20892

[2] NCI,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892

[3] NCI,REGISTRY EXPTL CANC,BETHESDA,MD

来源：

BLOOD | 1996年 / 87卷 / 04期

关键词：

D O I：

10.1182/blood.V87.4.1439.bloodjournal8741439

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Targeted disruption of the transforming growth factor-beta 1 (TGF-beta 1) gene in mice results in the development of a massive multifocal inflammatory disease in many tissues. Because no detectable pathogen was identified, we examined whether autoimmune mechanisms played a role in initiating or maintaining the inflammatory disease. The serum of TGF-beta 1 knockout mice contained elevated titers of antibodies to nuclear antigens (ssDNA, dsDNA, Sm, and RNP), as well as reactivity against the 16/6 idiotype (16/6 Id). In addition, Ig deposits were detected in renal glomeruli of TGF-beta 1 knockout mice. Transplantation of TGF-beta 1 knockout hematopoietic cells into normal irradiated recipients resulted in a similar profile of autoantibody production as well as in the induction of inflammatory lesions. Our results describe autoimmune activity that ensues when the TGF-beta 1 cytokine is absent. This is a US government work. There are no restrictions on ifs use.

引用

页码：1439 / 1445

页数：7

共 34 条

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