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The Journal of Immunology, 2004, 173: 3305-3309.
Copyright © 2004 by The American Association of Immunologists

TGF-{beta} Receptor Signaling Is Critical for Mucosal IgA Responses1

Stefan Borsutzky*, Balthazar B. Cazac{dagger}, Jürgen Roes2,{dagger} and Carlos A. Guzmán2,*

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

TGF-{beta} receptor (T{beta}R) 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 T{beta}R in B cells (T{beta}RII-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 T{beta}RII-B mice. However, a significant reduction in Ag-specific IgG2b and increased levels of IgG3 were observed in sera from T{beta}RII-B mice. Furthermore, Ag-specific IgA-secreting cells, serum IgA, and secretory IgA were undetectable in T{beta}RII-B mice. These results demonstrate the critical role played by T{beta}R in Ag-driven stimulation of secretory IgA responses in vivo.




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