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Does interleukin-2 abrogate peripheral immunologic self-tolerance in vivo?
J Allison1, W Heath, J F Miller
1Walter and Eliza Hall Institute of Medical Research, Post Office Royal Melbourne Hospital, Victoria, Australia.
Seminars in Immunology
|June 1, 1992
Summary
Interleukin-2 (IL-2) in pancreatic beta cells did not prevent autoimmune diabetes in mice. IL-2 requires T cell activation and cannot reverse established tolerance in this model.
Area of Science:
- Immunology
- Endocrinology
- Transgenic Models
Background:
- Pancreatitis and islet infiltration observed in RIP-IL-2 transgenic mice.
- Previous studies suggest IL-2's role in immune regulation.
Purpose of the Study:
- To investigate the effect of constitutive interleukin-2 (IL-2) expression in pancreatic beta cells on autoimmunity.
- To determine if IL-2 can overcome peripheral tolerance mechanisms.
Main Methods:
- Generation of RIP-IL-2 transgenic mice expressing murine IL-2 in islet beta cells.
- Analysis of immune cell infiltration and autoimmune responses in these mice.
- Coexpression of IL-2 with extrathymic H-2Kb molecules to study tolerance induction.
Main Results:
- RIP-IL-2 mice exhibited pancreatitis and islet infiltration but not islet autoimmunity.
- Coexpression of IL-2 and H-2Kb did not induce autoimmunity.
- IL-2 did not reverse tolerance in unresponsive T cells.
Conclusions:
- Constitutive IL-2 expression in beta cells does not induce islet autoimmunity.
- IL-2 appears to act primarily on activated T cells and cannot reverse established tolerance in this model.
- Peripheral tolerance mechanisms remain effective even with IL-2 presence.