Immune cells accumulate and promote bone loss in aging mice
Experiments in male mice identified a bone marrow B cell population that increased with age and caused bone loss when transferred into young mice.
Limit: The contribution of these B cells relative to other RANKL sources was not quantified
Edited by Boris Djordjevic · AgingResearch.News
In experiments in male C57B6 mice, researchers compared bone marrow from young and aged animals and tested a group of B cells, immune cells that make antibodies. These cells carried RANKL, a protein that promotes bone breakdown, and CXCR4, a receptor for chemical signals. They accumulated in aged mice and were a major source of RANKL in bone marrow.
Transferring these cells from aged mice into young NSG mice caused bone loss. The researchers also gave 22-month-old mice plerixafor, which blocks CXCR4, at 5 milligrams per kilogram of body weight daily for one month. Compared with mice given injections without the drug, these mice had fewer of the B cells in bone marrow and greater volume and thickness of spongy bone. Plerixafor also increased bone mass in mice whose ovaries had been removed.
Why it matters
The authors proposed reducing this bone marrow B cell population as a possible way to treat or prevent osteoporosis.
Caveats
These were mouse experiments, and the natural-aging comparisons used males. The authors noted that these B cells’ importance relative to other cellular sources of RANKL remained unclear.
The paper
Hebei Medical University; University of Rochester Medicine
Bone Research, May 18, 2026, Open access
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