Effect of iron deficiency on the response of mouse lymphocytes to concanavalin A: the importance of transferrin-bound iron.

The in vitro response to Con A of lymphocytes from iron-deficient and normal mice in media containing either 10% fetal calf serum, apotransferrin or 20% iron-saturated transferrin was similar for the iron-deficient and control groups. However, the degree of proliferation in serum-free medium containing apotransferrin was significantly lower in all groups, compared to the responses in media containing either 20% iron-saturated transferrin or 10% fetal calf serum. Proliferation of lymphocytes from normal, iron-deficient or iron-repleted mice was lower in media supplemented with serum from iron-deficient mice than when serum from normal or iron-repleted mice was used. Addition of sufficient iron to bring the iron level of the deficient serum to that of normal serum significantly improved its ability to promote proliferation, while in vivo repletion of iron-deficient mice resulted in a restoration of normal lymphocyte responses to Con A. The proportion of cells positive for Thy 1.2, Ly 1 and Ly 2 antigens did not differ significantly between any groups of mice. Protein synthesis by cells proliferating in serum-free medium containing apotransferrin or 20% iron-saturated transferrin was the same in all groups of mice. These results indicate that decreased lymphocyte proliferative responses in iron deficiency may be due to inadequate levels of circulating transferrin-bound iron, rather than to intrinsic defects in the cells themselves or changes in the proportions of different T-cell subsets, and that iron availability does not affect protein synthesis by proliferating lymphocytes.