MODULATION OF PROTEIN KINASE C (PKC) ISOENZYME PATTERN BYTHYROID AXIS IN NORMAL LYMPHOCYTES

KLECHA A.J.; BARREIRO ARCOS M.L.; STERLE H; GENARO A.M.; CREMASCHI G.A

Madrid

Congreso; 2nd Iberoamerican Congress on Neuroimmunomodulation; 2007

Neuroimmunomodulation International Society

Evidences pointing to bidirectional regulation between thy¬roid axis and the immune system were described. Previously we showed that T and B cells from hyperthyroid (HT) mice upon stimulation with mitogens showed higher stimulation indexes than control cells, while the contrary occurred with hypothyroid (ht) Iymphocytes. To characterize the biochemi¬cal mechanisms involved in these effects, PKC activity upon mitogen stimulation and the expression of crucial PKC isoen¬zyme that participate in T (a, b and q) and B (a, b, d and z ) Iymphocyte activation were evaluated. PKC total activity and mitogen-induced PKC translocation was increased in HT, but decreased in ht Iymphocytes. This was accompanied by an increment of a, b and q isoforms in T cells, but only b in B cells from HT mice. ln ht T Iymphocytes a decrease in b isoen¬zyme was found, while in B cells diminished expression of b and z isoforms were observed. Moreover, spleen cells from HT and ht mice stimulated in vitro with a T selective mitogen displayed a higher or lower IL-2 and IFN-y secretion respec¬tively, when compared to control euthyroid cells. No differ¬ences were found for IL-6 Ievels. Results indicate that thyroid status modify Iymphocyte activity through PKC isoenzyme regulation, thus leading to the modulation of Iymphoid cell proliferation and of important cytokines related to cellular immunity.