BAFF augments IgA2 and IL‐10 production by TLR7/8 stimulated total peripheral blood B cells

Abstract: Class‐switching of B cells to IgA can be induced via both T‐cell‐dependent and T‐cell‐independent mechanisms. IgA is most predominantly produced mucosally and is important for combating infections and allergies. In contrast to mice, humans have two forms of IgA; IgA1 and IgA2 with diverse tissue distribution. In early life, IgA levels might be sub‐optimal especially during the fall season when bacterial and viral infections are more common. Therefore, we investigated using human B cells whether T‐cell‐independent factors ‐promoting cell survival, class switching and immunoglobulin secretion‐ BAFF, APRIL, IL‐10 and retinoic acid can boost IgA production in the context of viral or bacterial infection. To this end total and naive peripheral blood B cells were stimulated with these factors for 6 days in the presence or absence of TLR7/8 agonist R848 (mimicking viral infection) or TLR9 agonist CpG‐ODN (mimicking bacterial infection). We show that BAFF significantly augments IgA2 production in TLR7/8 stimulated mature, but not naïve B cells. In addition, BAFF augments IL‐10 production and viability in TLR7/8 and TLR9 stimulated mature B cells. These data warrant further investigation of its role in immune regulation both in the periphery and mucosal tissues in early life or during disease.

Object Details

• Location: Deutsche Nationalbibliothek Frankfurt am Main
• Extent: Online-Ressource
• Language: Englisch

References and Relationships

• Bibliographic citation: BAFF augments IgA2 and IL‐10 production by TLR7/8 stimulated total peripheral blood B cells ; volume:48 ; number:2 ; year:2018 ; pages:283-292 ; extent:10 ; European journal of immunology ; 48, Heft 2 (2018), 283-292 (gesamt 10)

Contributors, Places and Time

• Creator: den Hartog, Gerco ; van Osch, Thijs L.J. ; Vos, Martijn ; Meijer, Ben ; Savelkoul, Huub F.J. ; van Neerven, R.J. Joost ; Brugman, Sylvia

Further information

• DOI: 10.1002/eji.201646861
• URN: urn:nbn:de:101:1-2022090608132125466079
• Rights: Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.
• Last update: 15.08.2025, 7:27 AM CEST