Artigo Acesso aberto Revisado por pares

Regulatory B cells from hilar lymph nodes of tolerant mice in a murine model of allergic airway disease are CD5+, express TGF-β, and co-localize with CD4+Foxp3+ T cells

2012; Elsevier BV; Volume: 5; Issue: 6 Linguagem: Inglês

10.1038/mi.2012.42

ISSN

1935-3456

Autores

P Natarajan, Anurag Singh, Jeff T. McNamara, Eric R. Secor, Linda Guernsey, Roger S. Thrall, Craig M. Schramm,

Tópico(s)

Immune Cell Function and Interaction

Resumo

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), transforming growth factor (TGF)-β-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 (Breg) 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, Breg in HLNs of LIT mice reside in a CD5+ TGF-β-producing subpopulation and co-localize with CD4+Foxp3+ T cells.

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