Expression of T lymphocyte p56(lck), a zinc-finger signal transduction protein, is elevated by dietary zinc deficiency and diet restriction in mice

Compromised immune function is common to Zn deficiency, protein and energy malnutrition; however, the causative mechanisms at the molecular level have not been elucidated. The T lymphocyte signal transduction pathway contains several Zn-finger proteins, and it is possible that the in vivo functionin g of these proteins could be affected by dietary deficiency of Zn and amino acids. Thus, the objective was to investigate the effects, on expression o f the T lymphocyte signal transduction proteins p56(lck), phospholipase C-g amma 1 (PLC gamma 1) and protein kinase C (PKC alpha), of dietary Zn defici ency (ZnDF, < 1 mg Zn/kg diet) and protein-energy malnutrition syndromes [2 % protein deficiency (LP), combined Zn and 2% protein deficiency (ZnDF+LP), and diet restriction (DR, body weight equal to ZnDF)] compared with contro l (C) mice. Indices of nutritional status and splenocyte counts were also d etermined. Based on serum albumin and liver lipid concentrations, the ZnDFLP and LP groups had protein-type malnutrition, whereas the ZnDF and DR gro ups had energy-type malnutrition. For Western immunoblotting of the signal transduction proteins, mouse splenic T lymphocytes were isolated by immunoc olumns. The expression of T lymphocyte p56(lck) was significantly elevated in the ZnDF+LP, ZnDF and DR groups compared to the C group. In contrast, th e expression of PLC gamma 1 and PKC was unaffected. There was a significant negative correlation between T lymphocyte p56(lck) expression and serum Zn (r = -0.65, P = 0.0007) or femur Zn (r = -0.73, P = 0.0001) concentrations . We propose that elevated T lymphocyte p56(lck) may contribute to altered thymoctye maturation, apoptosis and lymphopenia in Zn deficiency and protei n-energy malnutrition syndromes.