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.