Thyroid status influence lymphocyte activity via protein kinase C (PKC) isoenzyme modulation.

A KLECHA; M BARREIRO ARCOS; H STERLE; AM GENARO; G CREMASCHI

Córdoba, Argentina

Congreso; XXXVIII Reunión Anual de la SAFE; 2006

Sociedad Argentina de Farmacología Experimental

Evidences pointing to bidirectional regulation between thyroid 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) lymphocytes. To characterize the biochemical mechanisms involved in these effects,  PKC activity upon mitogen stimulation and the expression of crucial PKC isoenzyme that participate in T (a, b and q) and B (a, b, d and z) lymphocyte activation were evaluated. PKC total activity and mitogen-induced PKC traslocation was increased in HT, but decreased in ht lymphocytes. This was accompanied by an increment of  a, b and q  isoforms in T cells, but only b in B cells from HT mice. In ht T lymphocytes a decrease in b isoenzyme 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-g secretion respectively, when compared to control euthyroid cells. No differences were found for IL-6 levels. Results indicate that thyroid status modify lymphocyte activity through PKC isoenzyme regulation, thus leading to the modulation of lymphoid cell proliferation and of important cytokines related to cellular immunity.