Figure 8

IFNγ gene expression is modulated prior to experimental autoimmune encephalomyelitis (EAE) onset in the central nervous system (CNS) of immunized adults but not in neonates. To examine whether the T cells from neonates have the potential to differentiate into T helper (Th) effector populations that contribute to CNS autoimmunity in adult mice, highly purified CD4⁺CD62L⁺ naive T cells from neonates and adults were differentiated in vitro in the presence of either Th1 or Th17 inducing conditions. Relative mRNA expression for (A) IFNγ, and (B) IL-12 is shown. Data represent an average ± standard error of the mean (SEM) for three to seven CNS tissues/group. Tissues were collected at day 10 post immunization for EAE. In vitro, neonatal CD4⁺ T cells are as capable as adult CD4⁺ T cells of producing (C) IFNγ under Th1 polarizing conditions, and (D) IL-17 under Th17 polarizing conditions. Supernatants were collected at 48 hrs and 72 hrs and the levels IFNγ and IL-17 were determined by ELISA. (E) To quantify IFNγ expression in neonatal and mature encephalitogenic CD4⁺ T cells, lymph node cells were prepared for adoptive transfer as described above [22]. IFNγ expression was determined by ELISA after 24, 48, and 72 hrs in culture. At all time points, adult CD4⁺ T cells expressed significantly more IFNγ than neonatal CD4⁺ T cells.