Premium
Peripheral Blood Cells from Patients with Aplastic Anaemia in Partial Remission Suppress Growth of their Own Bone Marrow Precursors in Culture
Author(s) -
Nissen Catherine,
Cornu Pierre,
Gratwohl Alois,
Speck Bruno
Publication year - 1980
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.1980.tb07143.x
Subject(s) - bone marrow , immunology , granulocyte , medicine , cyclophosphamide , haematopoiesis , stem cell , biology , chemotherapy , microbiology and biotechnology
S ummary In 12 patients with severe aplastic anaemia who had achieved self‐sustaining autologous bone marrow function after treatment with antilymphocyte globulin, or with cyclophosphamide given for attempted bone marrow transplantation, colony formation by all haemopoietic precursors remained far below normal. Precursors from peripheral blood, erythroid precursors in particular, failed to form a normal number of colonies. This paucity of colony formation does not reflect a true lack of precursor cells but is due to circulating cells which impair maturation. Addition of low density peripheral blood cells to autologous bone marrow cultures diminished colony formation by granulocyte‐macrophage precursors (GM‐CFC) and abolished ‘burst’ formation by BFU‐E. Strong auto‐inhibition preceded relapse in four of eight patients. The phenomenon was not observed in five normals, in five aplastic anaemia patients with stable haemopoietic grafts and in three polytransfused control patients. The T‐cell poor subpopulation of peripheral blood cells, containing mainly B‐cells and macrophages, was especially inhibitory. Accordingly, removal of plastic adherent cells from bone marrow cell suspensions improved plating efficiency in aplastic anaemia patients, but not in normals. Isolated E‐rosette positive cells had no negative effect. Inhibition could only be demonstrated in the autologous situation. Colony formation by normal allogeneic peripheral blood precursors was not impaired by patient cells. The phenomenon is likely to reflect residual disease activity which is compensated in vivo but can be demonstrated in vitro. It may be of help in early recognition of patients who are at risk of relapse after autologous bone marrow reconstitution.