Mature bone marrow erythroid burst-forming units do not require T cells for induction of erythropoietin-dependent differentiation.

Abstract

Cell-cell interactions between mature T cells and peripheral blood null cells induce erythropoietin-stimulated differentiation of peripheral blood-derived erythroid progenitors. By the use of complement-fixing cytolytic murine hybridoma and antibody uniquely reactive with mature T lymphocytes, this dependence of immature peripheral blood erythroid burst-forming unit (BFU-E) differentiation upon mature T cells or a T cell conditioned medium is confirmed. By using the same antibody, it is demonstrated that the differentiation of mature bone marrow BFU-E does not require either mature T cells or lymphocyte mitogenic factor. These findings do not preclude the presence in the bone marrow of other cells, perhaps even immature T cells, that influence erythropoietin-dependent erythroid differentiation of mature marrow BFU-E.

T gamma (T gamma) cells suppress growth of erythroid colony-forming units in vitro in the pure red cell aplasia of B-cell chronic lymphocytic leukemia.

“…1) are consistent with the concept that the mature erythroid stem cells (CFU-E) can proliferate in the absence of T cells (25). CFU-E numbers were, in fact, increased after T cell depletion in normals, which may reflect some enrichment of CFU-E by the separation procedure.…”

Lymphocyte dysfunction in congenital hypoplastic anemia.

“…In further studies, they have indicated that T helper function for erythropoiesis was not deficient in their patients with congenital hypoplastic anemia (14). However, it is presently unclear whether T helper cells are even required for normal bone marrow, rather than peripheral blood, erythroid colony growth (18). In our own patients, addition of normal peripheral blood mononuclear cells to patients' bone marrows in erythroid cultures failed uniformly to improve the poor erythroid colony growth of the patients, arguing against a helper cell defect in our patients, and supportive of an intrinsic proliferative defect.…”

Evidence for genetic restriction in the suppression of erythropoiesis by a unique subset of T lymphocytes in man.

“…A complex T cell network has been found to regulate the immune response in man (53) and considerable data have implicated what is believed to be a T lymphocyte as an inducer of erythroid differentiation (5,6,29,54,55). In addition, normal Ty cells have been shown to suppress in vitro erythroid (6,36) and granulocyte (56) colony expression.…”