T cells and erythroid burst forming units in chronic lymphocytic leukemia

Substantial evidence exists indicating T cell abnormalities in chronic lymphocytic leukemia (CLL). There is also evidence that the T cell is an important source of burst promoting activity (BPA) for the peripheral blood (PB) erythroid burst forming unit (BFU-e). We studied the BPA of T cells and response of BFU-e in normals and untreated early stage B cell CLL patients in a methylcellulose colony assay. Normal null cell cultures grew significantly more BFU-e than CLL null cell cultures. Addition of autologous T cells to normal or CLL null cells significantly increased BFU-e only in normals. Allogeneic coculture of T cells from CLL patients with null cells from normals yielded normal responses of BFU-e in five of six cases. In contrast, allogeneic coculture of normal T cells with CLL null cells yielded a normal response in only one of six studies. Furthermore, adding increasing quantities of autologous or normal allogeneic T cells to CLL null cells did not augment the BFU-e response. Accounting for the expanded lymphocyte pool in CLL, BFU-e are decreased in concentration but the absolute number is normal or increased. The decrease in concentration could be secondary to expansion of the null cell fraction in CLL by pre-B cells. CLL T cells appeared to augment normal allogeneic PB BFU-e in a normal fashion, whereas, in several cases, CLL BFU-e were hyporesponsive to autologous or normal allogeneic T cells. It is therefore apparent that in untreated early stage B cell CLL, erythroid progenitor cells are present in the peripheral blood but are diluted in an expanded null cell compartment and may, in some cases, be hyporesponsive to T cell BPA. T cell BPA of CLL T cells in this early stage of disease is preserved.