IL-10 EXPRESSION IN THYROID-GLANDS - PROTECTIVE OR HARMFUL ROLE AGAINST THYROID AUTOIMMUNITY

IL-10 is a cytokine which not only suppresses cellular immunity but al so stimulates the humoral response. In certain animal models of autoim munity, IL-10 exerts a protective effect against auto-destruction. Thi s study was to ascertain whether there could be a role for IL-10 in hu man autoimmune thyroid disease. Total RNA was extracted from snap-froz en thyroid bloch from surgical specimens. Five 'normal', five multinod ular, six Graves and two Hashimoto thyroids (one euthyroid and one hyp othyroid) were studied. Approximately 7 mu g of total RNA from each gl and were reverse transcribed with oligo-dT primers. Pre-plateau semiqu antitative polymerase chain reaction (PCR) was performed with specific IL-10 primers. PCR products were run on a 1.5% agarose gel, blotted o nto a N-hybond nylon membrane, hybridized with a specific internal pro be labelled with gamma-P-32-ATP and autoradiographed. Statistical anal ysis of densitometric values showed significantly higher IL-10 levels in the autoimmune than in the non-autoimmune glands. In situ hybridiza tion and immunohistochemistry showed that the IL-10 message was locate d within the infiltrating lymphomononuclear cells. Histological analys is revealed that the autoimmune thyroids with the highest IL-IO levels were characterized by relevant degrees of B and T cell infiltration a nd also exhibited the greatest percentage of spontaneous HLA class LI expression on thyrocytes. IL-10 and neutralizing anti-IL-10 antibodies were not able to regulate in vitro spontaneous or interferon-gamma (I FN-gamma)/phytohaemagglutinin (PHA)-induced HLA class II on thyrocytes . We conclude that in active autoimmune thyroiditis, in addition to th e well documented production of Th1 cytokines, Th2-related lymphokines can be detected simultaneously. It can be envisaged that in this cond ition the role of IL-10 might be directed to the stimulation of B cell proliferation and antibody production rather than to the suppression of proinflammatory cytokine release.