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T Cells That
Prevent Murine Insulin-dependent Diabetes
By
From The Walter and Eliza Hall Institute of Medical Research, Royal Melbourne Hospital, Parkville
3050, Australia
Cellular immune hyporesponsiveness can be induced by the presentation of soluble protein antigens to mucosal surfaces. Most studies of mucosa-mediated tolerance have used the oral route of antigen delivery and few have examined autoantigens in natural models of autoimmune disease. Insulin is an autoantigen in humans and nonobese diabetic (NOD) mice with insulindependent diabetes mellitus (IDDM). When we administered insulin aerosol to NOD mice after the onset of subclinical disease, pancreatic islet pathology and diabetes incidence were both
significantly reduced. Insulin-treated mice had increased circulating antibodies to insulin, absent splenocyte proliferation to the major epitope, insulin B chain amino acids 9-23, which
was associated with increased IL-4 and particularly IL-10 secretion, and reduced proliferation
to glutamic acid decarboxylase, another islet autoantigen. The ability of splenocytes from insulin-treated mice to suppress the adoptive transfer of diabetes to nondiabetic mice by T cells of
diabetic mice was shown to be caused by small numbers of CD8 
T cells. These findings reveal a novel mechanism for suppressing cell-mediated autoimmune disease. Induction of regulatory CD8 T cells by aerosol insulin is a therapeutic strategy with implications for the prevention of human IDDM.
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