In a study on diabetes‑prone rats, giving the immune protein IL‑2 helped prevent diabetes in one rat strain but made it worse in another. The strain that got worse had higher natural levels of thymosin‑alpha‑1, while the strain that improved had lower levels. This hints that thymosin‑alpha‑1 might affect how the immune system influences diabetes, but the work is in rats and not directly usable for people.

Long-term treatment with recombinant interleukin-2 (IL-2) of diabetes-prone BB rats had contrasting effects in two different BB rat sublines. Diabetes development was enhanced in the subline with a low intrinsic diabetes risk and suppressed in the subline with a high diabetes risk. IL-2 treatment started between 35 and 42 days of age and lasted for 3 months. In subline 1, diabetes incidence increased from 23% to 53% (P less than 0.01), in subline 2 it decreased from 73% to 32% (P less than 0.01). The two sublines differed in serum levels of factors controlling IL-2 synthesis and activity. Mean IL-2 inhibitory activity was higher in subline 2 (between 140% and 290% of levels in subline 1, P less than 0.01). Conversely, mean concentrations of thymosin alpha 1 and beta 4 were higher in subline 1 (between 140% and 200% of levels in subline 2, P less than 0.01). Thus the two sublines differ in their response to exogenous IL-2 and also in serum levels of mediators affecting availability of IL-2. We conclude that an internal network of hormonal factors, including IL-2, contributes to the control of diabetes development in the BB rat.