No abstract

This study was conducted to further characterize the effector cells of experimental allergic encephalomyelitis (EAE) which are activated in vitro when spleen cells from Lewis rats previously immunized with myelin basic protein and adjuvant are cultured with antigen prior to transfer to syngeneic recipients. The effector cells were isolated on discontinuous Percoll gradients in the cell fraction that floated on Percoll with a buoyant density of 1.067 kg/l. These cells (designated fraction 1) transferred EAE and incorporated [3H]dThd in culture. Fraction 1 was enriched for T cells when evaluated with monoclonal anti-rat T cell serum W3/13 and deficient in Ig+ cells; approximately 33% were positive with monoclonal anti-rat T cell serum W3/25. In contrast, the small, nonproliferating cells found in higher density Percoll fractions did not transfer EAE. When fraction 1 was recultured in the presence of basic protein and interleukin 2 for 72 h, these cells retained the ability to transfer EAE. Moreover, these recultured cells exhibited an increase in the W3/25 antigen and a decrease in the W3/13 marker. It was concluded that a subset of T cells which bear the W3/25 marker is involved in the transfer of EAE.

Relatively low numbers of spleen and lymph node cells from Lewis rats previously challenged with myelin basic protein efficiently transfer experimental allergic encephalomyelitis (EAE) to normal syngeneic recipients after in vitro culture with antigen. Moreover, cells obtained from rats that have recovered and are resistant to EAE can also transfer disease. Cell separation studies show that a nylon wool-adherent cell is responsible for transfer of EAE. Density gradient ultracentrifugation revealed that these effector cells are probably lymphoblasts.

No abstract

No abstract