Abstract
Tolerance to the semi-allogenic fetal graft by the maternal immune system is a medical enigma. Many aspects of immunoregulation at the feto-maternal interface have been clarified, but systemic effects of pregnancy on the immune system are still elusive. The present study was undertaken to determine whether mid-pregnancy mouse serum has an inhibitory effect on dendritic cells (DC) function. Mid-gestational sera were obtained from allogenic pregnant Balb/c mice (Balb/c × C57BL/6) on days 9-11 of gestation. Splenic DC were purified from Balb/c mice, and treated with mid-pregnancy mouse serum. Antigen pulsed DC were injected into mice palms. After 5 days, draining lymph nodes were removed, cultured in the presence of cognate antigen, and proliferation of responding cells was measured by (3)H-thymidin incorporation. Interleukin (IL)-10 and interferon-gamma (IFN-γ) production by stimulated lymph node antigen-specific cells was also measured in culture supernatants using sandwich ELISA. Treatment of DC with pregnant mouse serum markedly blocked their ability to induce antigen-specific lymphocyte proliferation and IFN-γ and IL-10 production by primed lymph node cells in comparison with non-pregnant serum-treated DC. Pregnant mouse serum has an inhibitory effect on DC capacity to induce antigen-specific proliferation and cytokine secretion by lymph node cells. The suppressive effects of pregnant serum on DC could be considered as one of the mechanisms responsible for the systemic immunomodulation observed during pregnancy.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.