848 LOSS OF HELPER CELL FUNCTION IN AELASTIC ANEMIA

Abstract

Ficoll-Hypaque separated marrow cells from 16 patients and normal volunteers were cultured in soft agar for CFU-c (colony forming units). Marrow cells were further fractionated by velocity sedimentation at unit gravity. Fast sedimenting marrow fractions were cocultured with slowly sedimenting autologous and allogeneic lymphoid cell fractions for 24 hrs, and then plated in soft agar culture. Unfractionated marrow cells from AA patients failed to grow in soft agar. Findings suggestive of a loss of helper cell function were observed in 3 patients; results of one such patient are presented here. The myeloid fraction (sedimentation velocity 5-6.4 mm/hr) of the patient's marrow grew 6.5 colonies/105 cells. Coculture of this fast sedimenting fraction with slowly sedimenting normal allogeneic marrow cells (sedimentation velocity < 3mm/hr, morphologically small lymphocytes, no growth in soft agar) resulted in 42.5 colonies/105 cells, (i.e. 653% enhancement). In contrast, slowly sedimenting lymphoid cells from the patient's marrow failed to enhance colony formation of autologous myeloid marrow fractions. Thus, in addition to the previously described abnormalities in AA, helper cell defects may also exist in this disorder. Recovery of some patients following treatment with anti-thymocyte globulin and hemi-allogeneic marrow transplantation may be mediated by interaction of helper cells in the transplanted marrow with patient's own stem cells.