We found a match
Your institution may have access to this item. Find your institution then sign in to continue.
- Title
Co-activation through TLR4 and TLR9 but not TLR2 skews Treg-mediated modulation of Igs and induces IL-17 secretion in Treg:B cell co-cultures.
- Authors
Adjobimey, Tomabu; Satoguina, Judith; Oldenburg, Johannes; Hoerauf, Achim; Layland, Laura E
- Abstract
Whereas Th17 cells are associated with aggravated inflammation, regulatory T cells (Tregs) provide an environment to control overt responses. Nevertheless, Tregs display a certain degree of plasticity demonstrating that T cell differentiation processes are not absolute. Previously, we showed that human Treg clones induced B cells to produce IgG4. Here we focus on the actions of freshly isolated CD4+CD25+Foxp3+CD127dim Tregs on Ig production by B cells and the consequences of prior TLR activation of B cells. In the absence of TLR stimuli, Tregs, but not conventional T cells, dampened B cell proliferation, plasma cell formation and, with the exception of IgG4, all other Ig production. Although IgG4 levels were unchanged in total B cell:Treg co-cultures, levels were increased in Treg co-cultures of naive, but not memory, B cells. Triggering TLR on B cells skewed both Ig and cytokine secretion patterns and, surprisingly, Tregs within TLR4- and TLR9- but not TLR2-triggered B cell co-cultures up-regulated retinoic acid related orphan receptor (RORC) and produced IL-17. These data indicate that under conditions like bacterial or viral infections, B cells can escape Treg control, and provides an explanation as to why patients suffering from allergy or helminth infections display polar immunopathological symptoms despite being exposed to the same agent.
- Subjects
TOLL-like receptors; IMMUNOGLOBULINS; INTERLEUKIN-17; CO-cultures; INFLAMMATION; PHENOTYPIC plasticity; T cell differentiation; CD4 antigen
- Publication
Innate Immunity, 2014, Vol 20, Issue 1, p12
- ISSN
1753-4259
- Publication type
Article
- DOI
10.1177/1753425913479414