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J Immunol. 2004 Dec 1;173(11):6583-91.

Pax5-deficient mice exhibit early onset osteopenia with increased osteoclast progenitors.

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Department of Orthopaedics and Rehabilitation, Yale University School of Medicine, New Haven, CT 06510, USA.


Pax5 encodes BSAP, a member of the paired box domain transcription factors, whose expression is restricted to B lymphocyte lineage cells. Pax5(-/-) mice have a developmental arrest of the B cell lineage at the pro-B cell stage. We show here that Pax5(-/-) mice are severely osteopenic, missing 60% of their bone mass. The osteopenia can be accounted for by a >100% increase in the number of osteoclasts in bone measured histomorphometrically. This is not due to a lack of B cells, because other strains of B cell-deficient mice do not exhibit this phenotype. There was no difference in the number of osteoclasts produced in vitro by wild-type and Pax5(-/-) bone marrow cells. In contrast, spleen cells from Pax5(-/-) mice produce as much as five times the number of osteoclasts as control spleen cells. Culture of Pax5(-/-) spleen cells yields a population of adherent cells that grow spontaneously in culture without added growth factors for >4 wk. These cells have a monocyte phenotype, produce large numbers of osteoclasts when induced in vitro, and therefore are highly enriched in osteoclast precursors. These data demonstrate a previously unsuspected connection between B cell and osteoclast development and a key role for Pax5 in the control of osteoclast development.

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