EXOGENOUS ADMINISTRATION OF IL-1-ALPHA INHIBITS ACTIVE AND ADOPTIVE TRANSFER AUTOIMMUNE DIABETES IN NOD MICE

被引：25

作者：

FORMBY, B

JACOBS, C

DUBUC, P

SHAO, T

机构：

[1] Sansum Medical Research Foundation, Laboratory of Immunology, Santa Barbara, CA

[2] Immunex Research and Development Corporation, Seattle, WA

来源：

AUTOIMMUNITY | 1992年 / 12卷 / 01期

关键词：

CYTOKINE DEFICIENCY; SYSTEMIC IL-1 TREATMENT; INSULITIS; PATHOGENIC; POLYCLONAL CD4+8-; IL-1 PLEIOTROPIC EFFECTS;

D O I：

10.3109/08916939209146126

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Diabetes susceptibility in non-obese diabetic (NOD) mice may involve immune dysregulation resulting from cytokine deficiencies. The cytokine IL-1 plays a role in various immune as well as endocrine responses and may be hypoexpressed in NOD mice. Treatment with low levels of exogenous IL-1 a for 22 weeks prevented the naturally occurring insulitis and diabetogenic process in NOD mice during and at least 33 weeks after cessation of IL-1α treatment. Treatment with IL-1α also inhibited insulitis and hyperglycemia induced by adoptive transfer of pathogenic, polyclonal CD4+8- T cells. Even after islet-cell destruction, IL-1α injections in diabetic NOD mice normalized plasma glucose levels when administered in combination with insulin, whereas equivalent levels of IL-1α alone did not. Our studies support the hypothesis that IL-1α suppresses autoimmune diabetes and hyperglycemia in NOD mice by pleiotropic effects on both immune and metabolic systems. Thus, IL-1 treatment could clinically be an effective immunotherapeutic modality for autoimmune diabetes mellitus by suppressing early disease progression or normalize plasma glucose levels when insulin is present. © 1992 Informa UK Ltd All rights reserved: reproduction in whole or part not permitted.

引用

页码：21 / 27

页数：7

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