In our study, we have shown that the numbers of myeloid and plasmacytoid DCs in patients with SLE are the same as in previous reports. Furthermore, the same decrease of myeloid

and plasmacytoid DCs were observed in patients with SLE-merged secondary SS. Meanwhile, there were no significant differences in the number of myeloid and plasmacytoid DCs among SSc-merged secondary SS patients and RA-merged secondary SS patients, as well as SSc and RA patients. However, we found a direct correlation between the number of myeloid DCs and the time from the onset of Sicca syndrome in patients of secondary SS. A similar correlation was also observed in patients with primary SS. We also found a negative correlation between the number of blood myeloid DCs and the frequency of tissue-infiltrated DCs in both primary and secondary SS. Furthermore, in contrast to the early phase of primary SS, in the AP24534 purchase minor salivary glands of primary later-phase SS patients the mature DCs disappeared. These findings suggest that the reduction of myeloid DCs is a common finding in the early stage of PD0332991 Sicca syndrome and that myeloid DCs contribute to the critical and pathogenic roles of Sicca syndrome of SS. In this study we hypothesized

that preferential trafficking of myeloid DCs into salivary or lachrymal glands play essential roles in the pathogenesis of Sicca syndrome of primary and secondary SS by initiating Th1 immune responses. It has been reported that in patients in the later phase of SS, the percentage of infiltrating B cells within the salivary glands is increasing [24–26], suggesting that cell interaction between DCs and helper T cells is no longer required. Further detailed studies will be required to determine which antigens trigger DC-mediated immune responses in the salivary glands of SS patients. Our data

raise the possibility that the infiltration of myeloid DCs within salivary glands has been caused by the early onset of SS; meanwhile, retaining inflammation may require another mechanism in the later phase of SS. This work was supported by a Grant-in-Aid for Scientific Tryptophan synthase Research (C) (subject 11670466) from the Japan Society for the Promotion of Science. None of the authors have any conflict of interest with the subject matter or materials discussed in the manuscript. “
“Glucocorticoid (GC) is often given when preterm delivery is expected. This treatment is successful in stimulating the development of the fetal lung. However, reports and related research regarding the prolonged effects of prenatal GC on the development of immunity are very limited. Some data, derived from infants whose mothers were given immunosuppressants during pregnancy for the treatment of autoimmune disorders, suggest that prenatal exposure to GC may have only a limited effect on the development of the immune system. What is unknown is whether the immune modulation effects of prenatal GC might appear at a later childhood stage and beyond.