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*
Department of Microbiology and Immunology, University of North Carolina, Chapel Hill, NC 27599;
Department of Pathology, University of Florida, Gainesville, FL 32610; and
The Jackson Laboratory, Bar Harbor, ME 04609
Several studies have provided indirect evidence in support of a
role for 
cell-specific Th2 cells in regulating insulin-dependent
diabetes (IDDM). Whether a homogeneous population of Th2 cells having a
defined cell Ag specificity can prevent or suppress autoimmune
diabetes is still unclear. In fact, recent studies have demonstrated
that cell-specific Th2 cell clones can induce IDDM. In this study
we have established Th cell clones specific for glutamic acid
decarboxylase 65 (GAD65), a known cell autoantigen, from young
unimmunized nonobese diabetic (NOD) mice. Adoptive transfer of a
GAD65-specific Th2 cell clone (characterized by the secretion of IL-4,
IL-5, and IL-10, but not IFN-
or TGF-) into 2- or 12-wk-old NOD
female recipients prevented the progression of insulitis and subsequent
development of overt IDDM. This prevention was marked by the
establishment of a Th2-like cytokine profile in response to a panel of
cell autoantigens in cultures established from the spleen and
pancreatic lymph nodes of recipient mice. The immunoregulatory function
of a given Th cell clone was dependent on the relative levels of
IFN- vs IL-4 and IL-10 secreted. These results provide direct
evidence that cell-specific Th2 cells can indeed prevent and
suppress autoimmune diabetes in NOD mice.
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