A DONOR-DERIVED ASIALO-GM1-CELL GENESIS DURING SYSTEMIC GRAFT-VERSUS-HOST DISEASE( CELL INDUCES DEPRESSION OF B)

The nature of the effector cell(s) responsible for the depression of B -cell genesis in the bone marrow of mice undergoing systemic graft-ver sus-host disease (GVHD) has been examined. Donor C57BL/6 (B6) mice wer e treated in vivo with either a single injection of anti-asialo GM1 an tibody (anti-ASGM1) to eliminate naturally occurring (endogenous) ASGM 1+ cells or B6xAF(1) (B6AF(1)) lymphoid cells followed by anti-ASGM1 t o eliminate both endogenous and ''induced'' ASGM1+ cells. Lymphoid cel ls from donor mice after the elimination of endogenous ASGM1+ cells pr oduced severe GVHD and concomitant depression of B-cell genesis when i njected into B6AF(1) recipients. In contrast, cells from donors deplet ed of both the endogenous and inducible ASGM1+ populations did not cau se GVHD or depletion of B lineage cells in B6AF1 recipients but did de press B-cell genesis in B6C3F(1) mice. The ''induced'' ASGM1+ cells we re Thy 1+, but their elimination did not significantly alter either ov erall T-cell function or specific cytotoxic T-cell (CTL) reactivity ag ainst the sensitizing (B6AF(1)) strain. The results suggest that the e ffector cell responsible for the depression of B-cell genesis during s ystemic GVHD can be induced to express ASGM1, is strain-specific and T hy 1+; but is not a conventional CTL. (C) 1994 by The American Society of Hematology.