Partial splenectomy but not total splenectomy preserves immunoglobulin M memory B cells in mice.
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2011-09
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The mechanism by which partial splenectomy preserves splenic immune function is unknown. Immunoglobulin (Ig) M memory B cells are critical for the immune response against encapsulated bacteria and are reduced in asplenic patients, although it is unknown whether partial splenectomy can preserve memory B cells. We hypothesized that IgM memory B cells (murine B-1a cells) would be preserved after partial splenectomy but not after total splenectomy in mice.Methods
We performed total splenectomy (n = 17), partial splenectomy (n = 10), or sham laparotomy (n = 16) on C57BL/6J mice. Mice were killed on postoperative day 10 or 30, and peritoneal washings were analyzed by multiparameter flow cytometry for expression of murine B-1a cells (IgM(pos)IgD(dull)CD5(pos)B220(dull)).Results
We found that B-1a cells were significantly reduced after both total and partial splenectomies compared with sham laparotomy in the early postoperative period, although normal levels of B-1a cells returned by postoperative day 30 in mice undergoing partial splenectomy but not total splenectomy.Conclusion
Partial splenectomy but not total splenectomy preserves the B-1a B-cell population in mice within 30 days after surgery. Maintenance of these critical B cells may contribute to the preservation of a splenic-dependent immune response after partial splenectomy.Type
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Tracy, Elisabeth T, Karen M Haas, Tracy Gentry, Melissa Danko, Joseph L Roberts, Joanne Kurtzberg and Henry E Rice (2011). Partial splenectomy but not total splenectomy preserves immunoglobulin M memory B cells in mice. Journal of pediatric surgery, 46(9). pp. 1706–1710. 10.1016/j.jpedsurg.2011.04.020 Retrieved from https://hdl.handle.net/10161/24657.
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Scholars@Duke

Joseph Linton Roberts
My overall research interests are studying T cell development and defining the molecular bases of inherited immunodeficiency diseases. We are using standard candidate gene analysis approaches as well as new high throughput genome-wide sequencing, bioinformatics and functional screening in zebrafish and murine models in our work. Using these strategies we have recently reported a new molecular etiology of severe combined immunodeficiency (SCID), CD3 zeta chain deficiency. In collaboration with Dr. Wesley Burks we are also examining changes in T cell transcription patterns following treatment for peanut allergy using genome wide oligonucleotide microarrays.

Henry Elliot Rice
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