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

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作者
Mohan S. Maddur
Meenu Sharma
Pushpa Hegde
Emmanuel Stephen-Victor
Bali Pulendran
Srini V. Kaveri
Jagadeesh Bayry
机构
[1] Institut National de la Santé et de la Recherche Médicale Unité 1138,
[2] Centre de Recherche des Cordeliers,undefined
[3] Equipe 16- Immunopathology and Therapeutic Immunointervention,undefined
[4] Université Pierre et Marie Curie – Paris 6,undefined
[5] UMR S 1138,undefined
[6] Université Paris Descartes,undefined
[7] UMR S 1138,undefined
[8] Emory Vaccine Center,undefined
[9] Yerkes National Primate Research Center,undefined
[10] Emory University,undefined
[11] Université de Technologie de Compiègne,undefined
[12] International Associated Laboratory IMPACT (Institut National de la Santé et de la Recherche Médicale,undefined
[13] France - Indian Council of Medical Research,undefined
[14] India),undefined
[15] National Institute of Immunohaematology,undefined
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摘要
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.
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