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TGF- Receptor Signaling Is Critical for Mucosal IgA Responses¹

Stefan Borsutzky^*, Balthazar B. Cazac, Jürgen Roes^2, and Carlos A. Guzmán^2,*

^* Vaccine Research Group, Division of Microbiology, Gesellschaft für Biotechnologische Forschung-German Research Centre for Biotechnology, Braunschweig, Germany; and Department of Immunology and Molecular Pathology, Windeyer Institute of Medical Sciences, University College London, London, United Kingdom

TGF- receptor (TR) signaling is important for systemic IgA production; however, its contribution to IgA secretion at mucosal sites remained uncertain. This important question was addressed using mice lacking the TR in B cells (TRII-B). Although reduced, IgA-secreting cells and IgA were still present in the systemic and mucosal compartments. The adaptive immune response was investigated after oral or nasal immunization using adjuvants acting on different molecular targets, namely, the cholera toxin B subunit and the macrophage-activating lipopeptide-2. Efficient Ag-specific cellular and humoral responses were triggered both in controls and TRII-B mice. However, a significant reduction in Ag-specific IgG2b and increased levels of IgG3 were observed in sera from TRII-B mice. Furthermore, Ag-specific IgA-secreting cells, serum IgA, and secretory IgA were undetectable in TRII-B mice. These results demonstrate the critical role played by TR in Ag-driven stimulation of secretory IgA responses in vivo.

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