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The diabetic BB rat. Neither Th1 nor Th2?
D Bellgrau1, D Stenger, C Richards
1Barbara Davis Center for Childhood Diabetes, University of Colorado Health Sciences Center, Denver, USA.
Hormone and Metabolic Research = Hormon- Und Stoffwechselforschung = Hormones Et Metabolisme
|June 1, 1996
Summary
Researchers identified abnormal T cells in diabetic rats, suggesting a link between impaired T cell development and autoimmune type I diabetes. This finding sheds light on the mechanisms behind this complex autoimmune disease.
Area of Science:
- Immunology
- Autoimmunity
- Endocrinology
Background:
- Type I diabetes is an autoimmune disease where the body attacks its own insulin-producing cells.
- The BB rat is a widely used animal model for studying type I diabetes.
- T helper (Th) cells, specifically Th1 and Th2 subsets, play critical roles in immune regulation and autoimmunity.
Purpose of the Study:
- To identify and characterize T cells involved in causing autoimmune type I diabetes in BB rats.
- To investigate the Th1/Th2 paradigm in the context of autoimmune diabetes.
- To explore the role of p56lck in T cell development and autoimmunity.
Main Methods:
- Analysis of peripheral T cells in BB rats.
- Phenotypic characterization of T cells.
- Assessment of transcript expression for p56lck.
Main Results:
- A significant reduction in regulatory peripheral Th2 cells was observed.
- Remaining T cells exhibited an immature phenotype, not clearly Th1 or Th2.
- Abnormal transcript expression of p56lck was detected in BB peripheral T cells.
Conclusions:
- Impaired development of mature regulatory Th2 cells may contribute to type I diabetes.
- Abnormal p56lck expression could hinder regulatory T cell maturation and promote autoreactive T cell escape.
- These findings provide insights into the pathogenesis of autoimmune diabetes.