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Influence of T lymphocytes on hematopoiesis in a patient with T cell hypoplasia
Author(s) -
Hoffman Ronald,
Lu Li,
Jansen Jan,
Bruno Edward,
Brandt John,
Boral Leonard,
Cheung Killian
Publication year - 1988
Publication title -
american journal of hematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.456
H-Index - 105
eISSN - 1096-8652
pISSN - 0361-8609
DOI - 10.1002/ajh.2830270210
Subject(s) - hypoplasia , haematopoiesis , medicine , hematopoietic cell , immunology , biology , genetics , stem cell
In this communication, we describe an unusual patient with a reported lifelong history of anemia. Investigation of the pathogenesis of this patient's bone marrow failure provided an interesting opportunity to determine the role of T cells in the regulation of human blood cell production. Phenotyping of the patient's mononuclear cells revealed severe T cell hypoplasia in both the peripheral blood and bone marrow. The patient's bone marrow was capable of producing 50–60% of the normal numbers of burst‐forming units—erythroid (BFU‐E) in the presence of optimal concentrations of erythropoietin, suggesting that marrow BFU‐E formation is in part independent of T cells. Addition of small numbers of class I identical donor T cells enhanced BFU‐E cloning efficiency to a level observed in normal controls. This enhancing effect was supplied by a T4 + (CD4) population of donor cells. The addition of donor T cells partially corrected the inability of patient marrow cells to produce megakaryocyte and mixed colonies. These studies suggest that prolonged T cell hypoplasia might deprive marrow progenitor and stem cells of a necessary enhancing effect that is required for sustained normal hemato‐poiesis. Such a T cell defect in rare instances may result in bone marrow failure.