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Human B cells induce dendritic cell maturation and favour Th2 polarization by inducing OX-40 ligand

Mohan S. Maddur, Meenu Sharma, Pushpa Hegde, Emmanuel Stephen-Victor, Bali Pulendran, Srini V. Kaveri and Jagadeesh Bayry ()
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Mohan S. Maddur: Institut National de la Santé et de la Recherche Médicale Unité 1138
Meenu Sharma: Institut National de la Santé et de la Recherche Médicale Unité 1138
Pushpa Hegde: Institut National de la Santé et de la Recherche Médicale Unité 1138
Emmanuel Stephen-Victor: Institut National de la Santé et de la Recherche Médicale Unité 1138
Bali Pulendran: Emory Vaccine Center, Yerkes National Primate Research Center, Emory University
Srini V. Kaveri: Institut National de la Santé et de la Recherche Médicale Unité 1138
Jagadeesh Bayry: Institut National de la Santé et de la Recherche Médicale Unité 1138

Nature Communications, 2014, vol. 5, issue 1, 1-13

Abstract: Abstract Dendritic cells (DCs) play a critical role in immune homeostasis by regulating the functions of various immune cells, including T and B cells. Notably, DCs also undergo education on reciprocal signalling by these immune cells and environmental factors. Various reports demonstrated that B cells have profound regulatory functions, although only few reports have explored the regulation of human DCs by B cells. Here we demonstrate that activated but not resting B cells induce maturation of DCs with distinct features to polarize Th2 cells that secrete interleukin (IL)-5, IL-4 and IL-13. B-cell-induced maturation of DCs is contact dependent and implicates signalling of B-cell activation molecules CD69, B-cell-activating factor receptor, and transmembrane activator and calcium-modulating cyclophilin ligand interactor. Mechanistically, differentiation of Th2 cells by B-cell-matured DCs is dependent on OX-40 ligand. Collectively, our results suggest that B cells have the ability to control their own effector functions by enhancing the ability of human DCs to mediate Th2 differentiation.

Date: 2014
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:5:y:2014:i:1:d:10.1038_ncomms5092

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DOI: 10.1038/ncomms5092

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