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International Immunology Advance Access originally published online on September 26, 2005
International Immunology 2005 17(11):1495-1503; doi:10.1093/intimm/dxh327
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© The Japanese Society for Immunology. 2005. All rights reserved. For permissions, please e-mail: journals.permissions@oupjournals.org

Partial rescue of B cells in microphthalmic osteopetrotic marrow by loss of response to type I IFNs

Kirstin M. Roundy1, Gerald Spangrude2, Janis J. Weis1 and John H. Weis1

1 Department of Pathology and 2 Department of Medicine, University of Utah School of Medicine, 50 N Medical Drive, Salt Lake City, UT 84132, USA

Correspondence to: J. H. Weis; E-mail: john.weis{at}path.utah.edu

The microphthalmic (mi) mouse exhibits deficiencies in the development of osteoclasts, melanocytes, mast cells and marrow B cells. Previously, we demonstrated that the marrow of such mice over-express receptor activator of nuclear factor {kappa}B (RANK) ligand (RANKL). RANKL has been shown to induce the production of IFN-ß, a type I IFN. Additionally, maturing B cells have been shown to undergo apoptosis in response to type I IFNs including IFN-ß during differentiation. We hypothesized that the loss of B cells in the marrow of mi mice was due to the over-expression of IFN-ß as a result of heightened RANK–RANKL signaling. Creating a mouse with the mi genotype that was non-responsive to IFN-ß (lacking the type I IFNR) allowed us to test this hypothesis. These mice demonstrated an elevated number of marrow B cells and marrow precursor cells compared with mi animals possessing the type I IFNR. Intriguingly, type I IFNR-deficient wild-type animals also demonstrated an increased number of precursor cells in the marrow, but not an expansion of B220-positive pre-B cells, compared with wild type, suggesting that modulation of type I IFN responses directly controls the development of marrow constituents.

Keywords: B cells, microphthalmic, interferon, marrow, RANK/RANKL, mouse

Transmitting editor: T. Tedder


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