Pregnancy Modulates Adoptively Transferred Experimental Autoimmune Encephalomyelitis (EAE)

Abstract

Pregnancy affects the clinical course of autoimmune disease such as multiple sclerosis (MS), Rheumatoid arthritis and lupus. In this study, we determined the immunoregulatory role of pregnancy on the effector phase of murine experimental autoimmune encephalomyelitis (EAE), a model for studying MS. We used an adoptive transfer system with myelin basic protein (MBP) peptide NAc1‐11 activated Th1 or Th17 MBP T cell receptor (TCR) transgenic (Tg) donor cells. Transfer of activated Th1 cells to recipients during mid pregnancy resulted in EAE with a delayed onset and reduced clinical severity. No significant differences in EAE were observed when Tg cells transferred into late pregnant or post partum recipients compared with virgin controls. Mice during mid pregnancy produced less Th1 cytokines (IFN‐gamma and IL‐2) but increased IL‐10. In contrast, mice during post partum produced more Th1 and Th17 cytokines. No differences were noted in Foxp3 regulatory cells or Th2 cytokine production. These results suggest that mid pregnancy provides an immunoregulatory environment that suppresses Th1‐induced EAE (Supported by NIH grant AI 43376).