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Autoantibodies inhibit interleukin-7-mediated proliferation and are
associated with the age-dependent loss of pre-B cells in autoimmune New
Zealand Black Mice
MS Merchant, BA Garvy and RL Riley
Department of Microbiology and Immunology, University of Miami School of
Medicine, Florida 33101, USA.
Surface IgM+B220+ B cell precursors can be categorized as either
leukosialin (CD43/S7) negative (late stage pre-B cells) or positive
(pro-B/early pre-B cells). In autoimmune New Zealand Black (NZB) mice, bone
marrow small pre-B cells (IgM-CD43-B220+) and pro-B/early pre-B cells
(IgM-CD43+B220+) declined significantly with age. In particular,
subpopulations of pro-B/early pre-B cells expressing the heat stable
antigen (HSA) were found in lower proportions with age. Significant
decreases in interleukin-7 (IL-7) colony forming units (CFU) were also seen
in NZB mice by 6 to 8 months of age and accompanied alterations in the
numbers of pro-B and pre-B cells in bone marrow. Concomitant with reduced
numbers of B lineage precursor cells and IL-7 CFU in vivo, NZB mice
produced serum IgM antibodies that strongly inhibited IL-7 CFU responses in
vitro. Two monoclonal IgM antibodies (5G9, 2F5) derived from LPS stimulated
10-month-old NZB splenocytes recognized pre-B cell surface antigens on both
pre-B cell lines and on IL-7 stimulated bone marrow pro-B/pre-B cells.
However, these monoclonal antibodies (MoAb) failed to significantly stain
ex vivo bone marrow cells. The 5G9 and 2F5 MoAbs also partially inhibited
IL-7 CFU in vitro. These results suggest that NZB bone marrow becomes
increasingly deficient in B cell precursors and especially in IL-7
responsive pre-B cells with age. IgM serum antibodies and monoclonal IgM
antibodies derived from older NZB mice inhibit pre-B cell growth to IL-7.
The production of such autoantibodies may interfere with B cell development
in aging NZB mice by preventing IL-7-mediated proliferation.
Volume 87,
Issue 8,
pp. 3289-3296,
04/15/1996
Copyright © 1996 by The American Society of Hematology
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