Session: FP28-Thyroid Autoimmunity
Room 103 (Moscone Center)
Poster Board SUN-437
Methods.The effects of increasing concentrations of corticosteroids or rapamycin, on Th1 [chemokine (C-X-C motif) ligand 10 (CXCL10)] and Th2 [chemokine (C-C motif) ligand 2 (CCL2)] secretion in primary cultures of fibroblasts, preadipocytes and myoblasts from the orbits of GO patients were tested.
Results.In primary cultures of fibroblasts, preadipocytes and myoblasts from GO patients, CXCL10 was undetectable in the supernatant, while low amounts of CCL2 were produced basally. Interferon(IFN)-gamma dose-dependently induced CXCL10 release, while had no effect on CCL2 secretion. Tumor necrosis factor(TNF)-alpha dose-dependently induced CCL2 release, but had no effect on CXCL10 secretion. However, the combination of TNF-alpha and IFN-gamma had a significant synergistic effect on both CXCL10 and CCL2 chemokines secretion. Increasing concentrations of corticosteroids or rapamycin (in a pharmacological range), added at the time of IFN-gamma and TNF-alpha stimulation, dose-dependently inhibited both CXCL10 and CCL2 release in GO fibroblasts, preadipocytes and myoblasts in primary cultures.
Conclusion.Corticosteroids or rapamycin, in a pharmacological range, play an inhibitory role both on Th1 (CXCL10) and Th2 (CCL2) chemokines, in GO orbital cells, suggesting the therapeutic effect of these drugs could be exerted, at least in part, through this mechanism.
Nothing to Disclose: AA, SMF, PF, IR, AD, SS, EF
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