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a Departments of Oncology and
b Pediatrics, Johns Hopkins University School
of Medicine, Baltimore, Maryland, USA
Key Words. CD34+ cells • NOD/SCID chimeras • Xenogeneic stem cell transplantation • Lymphopoiesis • CD5+ B cells • Immunophenotyping • Hematopoiesis
Dr. Curt I Civin, Oncology 3-109, Johns Hopkins Hospital, 600 N. Wolfe Street, Baltimore, Maryland 21287-5001, USA.
The nonobese diabetic/severe combined immunodeficient (NOD/SCID)
xenotransplantation model is increasingly utilized to study both human
lymphohematopoietic stem/progenitor cells and committed cell
types. Human B lymphoid cells develop and proliferate in this
model. We found high numbers of CD19+CD5+ B
lymphoid cells in the bone marrows and spleens of NOD/SCID mice
transplanted with human CD34+ stem/progenitor cells. The
CD5+ cells accounted for a particularly large percentage of
the B lymphoid cells in the spleens of chimeras analyzed three months
after transplantation. CD19+CD5+ cells from all
the analyzed chimeras coexpressed HLA-DR, surface IgM, CD20, CD38,
CD43, and CD45. However, CD19+CD5+ cells were
negative for
light chain, CD10, CD11a, CD11b, CD15, CD21,
CD22, CD23, CD25, CD34, CD35, CD44, CD62L, CD69, and CD71. Cell
surface expression of the 
light chain, surface IgD, CD9, and
CD40 antigens was detected in some but not all chimeras. Thus, the
CD19+CD5+ cell population detected in our study
has the phenotype of previously described CD5+ B lymphoid
cells in humans and other species. The origin and role of the B
lymphoid cells which express CD5 cell surface glycoprotein are poorly
understood. The malignant cells in B lymphoid chronic lymphocytic
leukemia express CD5, and the numbers of CD5+ B lymphoid
cells are elevated in several autoimmune conditions. The
human-NOD/SCID chimera system may provide an in vivo model to
investigate the maturation and development of this cryptic human
CD5+ B lymphoid cell subpopulation.
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