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Blood, 15 January 2006, Vol. 107, No. 2, pp. 835-840.
Prepublished online as a Blood First Edition Paper on September 22, 2005; DOI 10.1182/blood-2005-07-2705.
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Submitted July 7, 2005
Accepted September 14, 2005
Beta-glucan enhances complement-mediated hematopoietic recovery after bone marrow injury
Daniel E Cramer, Daniel J Allendorf, Jarek T Baran, Richard Hansen, Jose Marroquin, Bing Li, Janina Ratajczak, Mariusz Z Ratajczak, and Jun Yan*
Tumor Immunobiology Program and Stem Cell Biology Program, James Graham Brown Cancer Center, University of Louisville, Louisville, KY, USA
* Corresponding author; email: jun.yan{at}louisville.edu.
Myelotoxic injury in the bone marrow (BM) as a consequence of total body irradiation (TBI) or granulocyte colony stimulating factor (G-CSF) mobilization results in the deposition of iC3b on BM stroma (stroma-iC3b). In the present study, we have examined how stroma-iC3b interacts with hematopoietic progenitor cells (HPC) and the role of complement (C) and complement receptor 3 (CR3) in BM injury/repair. We demonstrate here that stroma-iC3b tethers HPC via the inserted (I)-domain of HPC complement receptor 3 (CR3, CD11b/CD18, Mac-1). Following irradiation, stroma-iC3b was observed in the presence of purified IgM and normal mouse serum (NMS), but not serum from Rag-2-/- mice, implicating a role for antibody (Ab) and the classical pathway of C activation. Furthermore, a novel role for soluble yeast  -glucan, a ligand for the CR3 lectin-like domain (LLD), in the priming of CR3+ HPC is suggested. Soluble yeast -glucan could enhance the proliferation of tethered HPC, promote leukocyte recovery following sub-lethal irradiation, and increase the survival of lethally-irradiated animals following allogeneic HPC transplantation in a CR3-dependent manner. Taken together, these observations suggest a novel role for C, CR3, and -glucan in the restoration of hematopoiesis following injury.
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