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Accelerated Type 1 Diabetes Induction in Mice by Adoptive Transfer of Diabetogenic CD4+ T Cells

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Type 1 diabetes induction in humanized mice.

Shulian Tan^1,2,3,4, Yang Li^1,2,3,4, Jinxing Xia⁴

¹The First Hospital, Jilin University, Changchun, China 130061.

Proceedings of the National Academy of Sciences of the United States of America

|September 7, 2017

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This summary is machine-generated.

A new humanized mouse model lacking graft-versus-host reactivity enables studying type 1 diabetes pathogenesis. This model demonstrates how specific T cells cause beta-cell destruction, paving the way for antigen-specific therapies.

Area of Science:

Immunology
Endocrinology
Transplantation

Background:

Type 1 diabetes (T1D) research needs better humanized in vivo models for studying immune responses and developing antigen-specific therapies.
Current models are limited by xenogeneic graft-versus-host reactivity, hindering autoimmunity assessment.
Identifying human T cells and autoantigens involved in beta-cell destruction is crucial for T1D immunopathogenesis.

Purpose of the Study:

To develop and validate a humanized mouse model (hu-mice) that mimics T1D immunopathogenesis without xenogeneic graft-versus-host reactivity.
To investigate the role of specific human CD4+ T cells in initiating and driving autoimmune diabetes.
To assess the potential of this model for preclinical testing of T1D immunotherapies.

Main Methods:

Keywords:

humanized mice insulin type 1 diabetes

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Constructed hu-mice by transplanting human fetal thymus and CD34+ cells into HLA-DQ8-transgenic immunodeficient mice.
Induced diabetes by transferring autologous HLA-DQ8/InsB:9-23-specific T-cell receptor (TCR)-expressing CD4+ T cells and immunizing with InsB:9-23.
Administered streptozotocin to stress pancreatic islets and observed T cell infiltration and insulitis.

Main Results:

Hu-mice developed hyperglycemia and diabetes following transfer of specific T cells and immunization.
Infused human T cell survival was dependent on the host's preexisting human immune system.
Pancreatic infiltration by human CD3+ T cells and insulitis were observed in diabetic hu-mice with stressed islets.

Conclusions:

This study establishes a pathogenic role for islet autoreactive CD4+ T cell responses in human T1D induction, fitting Koch's postulates.
The model demonstrates that disease can be initiated by T cells recognizing specific epitopes (InsB:9-23) in the context of islet inflammation.
This preclinical hu-mouse model is valuable for studying T1D pathogenesis and evaluating targeted immunotherapies.