Bone Loss and TLR4 Signals Contribute Independently to B Lineage Aging.

Erin Baker, Encarnacion Montecino-Rodriguez, Shili Xu, Sotirios Tetradis, Adrien Rouault, Oscar I Estrada, Kenneth Dorshkind

Departments of Pathology and Laboratory Medicine, UCLA School of Dentistry, Los Angeles, California, USA.Departments of Pathology and Laboratory Medicine, UCLA School of Dentistry, Los Angeles, California, USA. · pubmed

Paper

Abstract

B cell development declines with age, but how structural changes in the marrow environment contribute to that process is incompletely understood. Multiplexed volumetric imaging revealed that B lineage cells were enriched near bone, and trabecular bone in particular, in young mice. However, B cell progenitors were depleted from these regions in strains of old mice that exhibited senile osteoporosis. In striking contrast, the age-related decline of B lymphopoiesis was attenuated in mice in which bone mass was maintained over the lifespan and could be completely abrogated by concomitantly blocking TLR4 signaling. In addition to demonstrating that developing B lineage cells are not randomly distributed in the marrow, these results indicate that the age-related decline in B lymphopoiesis is influenced by the loss of salutary and not just an increase in inhibitory signals.

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Research summary

The paper claims that the age-related decline in B lymphopoiesis is influenced by the loss of supportive signals from the bone microenvironment and can be mitigated by blocking TLR4 signaling. This research is relevant as it explores mechanisms underlying aging processes and potential interventions that could enhance immune function in the elderly, addressing root causes of age-related decline rather than merely treating symptoms.

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