Studies in the NOD mouse model suggest that development of
diabetes mellitus type I can be prevented and established disease cured by deviation towards a Th2-type response. To obtain insight into whether this approach may be applicable to human disease, we investigated the Th1/Th2 cytokine balance in pancreatic tissue from two patients with diabetes of recent onset (Case 1, accidental death; Case 2,
ketoacidosis). Using the polymerase chain reaction to amplify reverse-transcribed
cDNA, signals for actin and CD36 confirmed
mRNA integrity and the presence of T cells in pancreatic tissue from both patients and from a control. IFN-gamma
cDNA was also amplified from all three tissues. However,
IL-4 (but not IL-10)
cDNA, was amplified from the pancreas of Case 1. Conversely,
IL-10 (but not IL-4)
cDNA was amplified from the the pancreas of Case 2. The control pancreas yielded specific signals for both
IL-4 and
IL-10. Our data extend the limited database on Th1 and Th2
cytokine expression in human pancreatic tissue from recently diagnosed diabetics. Moreover, together with previous observations, our findings raise the possibility that the lack of both
IL-4 and
IL-10 may be associated with the development of
IDDM in humans.