Regulatory b cells from hilar lymph nodes of tolerant mice in a murine model of allergic airway disease are cd5+, express tgf-beta, and co-localize with cd4+foxp3+ t cells. Mucosal Immunol

In a biphasic, ovalbumin (OVA)-induced murine asthma model where allergic airway disease is followed by resolution and the development of local inhalational tolerance (LIT), TGFβ-expressing CD5+ B cells were selectively expanded locally in hilar lymph nodes (HLN) of LIT mice. LIT HLN CD5+ B cells but not LIT HLN CD5 − B cells induced expression of Foxp3 in CD4+ CD25 − T cells in vitro. These CD5+ regulatory B cells and CD4+Foxp3+ T cells demonstrated similar increases in expression of chemokine receptors (CXCR4 and CXCR5) and co-localized in HLN B cell zones of LIT mice. The adoptive transfer of LIT HLN CD5+ B cells, but not LIT HLN CD5 − B cells, increased the number of CD4+Foxp3+ T cells in the lung and inhibited airway eosinophilia in this OVA model. Thus, regulatory B cells in HLNs of LIT mice reside in a CD5+ TGFβ-producing subpopulation and co-localize with CD4+Foxp3+ T cells