Rapid Publications p2-Microglobulin-Deficient NOD Mice Do Not Develop Insulitis or Diabetes

نویسندگان

  • LINDA S. WICKER
  • EDWARD H. LEITER
  • JOHN A. TODD
  • ROBERT J. RENJILIAN
  • ERIN PETERSON
  • LAURENCE B. PETERSON
چکیده

The role of CD8 T-cells in the development of diabetes in the nonobese diabetic (NOD) mouse remains controversial. Although it is widely agreed that class II-restricted CD4 T-cells are essential for the development of diabetes in the NOD model, some studies have suggested that CD8 T-cells are not required for p-cell destruction. To assess the contribution of CD8 T-cells to diabetes, we have developed a class of NOD mouse that lacks expression of p2-microglobulin (N0D-S2m). NOD-S^m""" mice, which lack both class I expression and CD8 T-cells in the periphery, not only failed to develop diabetes but were completely devoid of insulitis. These results demonstrate an essential role for CD8 T-cells in the initiation of the autoimmune response to p-cells in the NOD mouse. Diabetes 43:500-504, 1994

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Major histocompatibility complex class I-deficient NOD-B2mnull mice are diabetes and insulitis resistant.

Specific allelic combinations within the class II region of the major histocompatibility complex (MHC) represent a major genetic component for susceptibility to autoimmune insulin-dependent diabetes mellitus (IDDM) in humans. We produced and used a stock of NOD/Lt mice congenic for a functionally inactivated beta 2-microglobulin (B2mnull) locus to assess whether there was an absolute requiremen...

متن کامل

Intrinsic defects in the T-cell lineage results in natural killer T-cell deficiency and the development of diabetes in the nonobese diabetic mouse.

T-cell-mediated autoimmune diabetes in nonobese diabetic (NOD) mice is closely associated with natural killer T (NKT)-cell deficiency. To determine whether intrinsic defects of the T-cell lineage contribute to the pathogenesis of the disease and NKT cell deficiency, we reconstituted the T-cell compartment in NOD.scid or BALB.scid mice with T-cells from NOD, nonobese diabetes-resistant (NOR), or...

متن کامل

Direct evidence for the contribution of B cells to the progression of insulitis and the development of diabetes in non-obese diabetic mice.

The non-obese diabetic (NOD) mouse is an excellent animal model of autoimmune diabetes associated with insulitis. The progression of insulitis causes the destruction of pancreatic beta cells, resulting in the development of hyperglycemia. Although it has been well documented that T cells are required for the development of insulitis and diabetes in NOD mice, the importance of B cells remains un...

متن کامل

I-E+ nonobese diabetic mice develop insulitis and diabetes

The development of type I diabetes in the nonobese diabetic (NOD) mouse is under the control of multiple genes, one or more of which is linked to the major histocompatibility complex (MHC). The MHC class II region has been implicated in disease development, with expression of an I-E transgene in NOD mice shown to provide protection from insulitis and diabetes. To examine the effect of expressin...

متن کامل

Beta cells cannot directly prime diabetogenic CD8 T cells in nonobese diabetic mice.

Type 1 diabetes (T1D) is caused by the destruction of insulin-producing islet beta cells. CD8 T cells are prevalent in the islets of T1D patients and are the major effectors of beta cell destruction in nonobese diabetic (NOD) mice. In addition to their critical involvement in the late stages of diabetes, CD8 T cells are implicated in the initiation of disease. NOD mice, in which the beta2-micro...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:

دوره   شماره 

صفحات  -

تاریخ انتشار 2010