IL-10 critically modulates B cell responsiveness in rankl-/- mice

Veronica Marrella, Nadia Lo Iacono, Elena Fontana, Cristina Sobacchi, Heiko Sic, Francesca Schena, Lucia Sereni, Maria Carmina Castiello, Pietro Luigi Poliani, Paolo Vezzoni, Barbara Cassani, Elisabetta Traggiai, Anna Villa

Research output: Contribution to journalArticlepeer-review


The immune and the skeletal system are tightly interconnected, and B lymphocytes are uniquely endowed with osteo-interactive properties. In this context, receptor activator of NF-κB (RANK) ligand (RANKL) plays a pivotal role in lymphoid tissue formation and bone homeostasis. Although murine models lacking RANK or RANKL show defects in B cell number, the role of the RANKL-RANK axis on B physiology is still a matter of debate. In this study, we have characterized in detail B cell compartment in Rankl-/- mice, finding a relative expansion of marginal zone B cells, B1 cells, and plasma cells associated with increased Ig serum levels, spontaneous germinal center formation, and hyperresponse to CD40 triggering. Such abnormalities were associated with an increased frequency of regulatory B cells and augmented B cell-derived IL-10 production. Remarkably, in vivo IL-10-R blockade reduced T cell-triggered plasma cell differentiation and restrained the expansion of regulatory B cells. These data point to a novel role of the RANKL-RANK axis in the regulation of B cell homeostasis and highlight an unexpected link between IL-10 CD40 signaling and the RANKL pathway.

Original languageEnglish
Pages (from-to)4144-4153
Number of pages10
JournalJournal of Immunology
Issue number9
Publication statusPublished - May 1 2015

ASJC Scopus subject areas

  • Immunology
  • Medicine(all)


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