Deficiency of contrasuppressor lymphocytes in alloxan-diabetic mice

Abstract

Ly 1 immune cells of alloxan diabetic mice are inferior to cells of normoglycemic PCI sensitized animals in transferring adoptive responses into recipients. A new regulatory activity, contrasuppression, that prevents suppressor cells from influencing activity of immune cells, has been recently described. Two types of Ly 1 contrasuppressor (Tcs) cells modulate contact sensitivity reactions in mice. A non-specific Tcs cell, which by itself has no immune activity, helps Ly 1 immune effector cells in adoptive transfer to bypass, in the recipient, the suppressor cell barrier. The antigen-specific Tcs cell induced by immune complexes makes Ly 1 effector cells resistant to specific suppression. Both Tcs cells, in contrast to Ly 1 effector cells, adhere to Vicia villosa lectin and can easily be separated (VV + and VV −, respectively). Our experiments show that diabetic mice are deficient in nonspecific Tcs cells. The most important finding was that when immune Ly 1 cells of diabetic mice, which otherwise transfer little immunity, were injected together with Ly 1 VV + cells of normoglycemic animals (these cells have no ability to transfer immunity whatsoever), the adoptive transfer was significantly augmented. We also demonstrate that diabetic mice are unable, upon appropriate immunization, to produce antigen-specific Tcs cells. Since a hypoinsulinemic environment abolishes the function of promiscuous Tcs cells and prevents the development of antigen-specific Tcs cells, this may suggest that contrasuppressor cells have insulin receptors which make them particularly sensitive to insulin deficiency.