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Macrophages induce differentiation of plasma cells through CXCL10/IP-10

In tonsils, CD138(+) plasma cells (PCs) are surrounded by CD163(+) resident macrophages (Mϕs). We show here that human Mϕs (isolated from tonsils or generated from monocytes in vitro) drive activated B cells to differentiate into CD138(+)CD38(++) PCs through secreted CXCL10/IP-10 and VCAM-1 contact....

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Detalles Bibliográficos
Autores principales: Xu, Wei, Joo, HyeMee, Clayton, Sandra, Dullaers, Melissa, Herve, Marie-Cecile, Blankenship, Derek, De La Morena, Maria Teresa, Balderas, Robert, Picard, Capucine, Casanova, Jean-Laurent, Pascual, Virginia, Oh, SangKon, Banchereau, Jacques
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Rockefeller University Press 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3457728/
https://www.ncbi.nlm.nih.gov/pubmed/22987802
http://dx.doi.org/10.1084/jem.20112142
Descripción
Sumario:In tonsils, CD138(+) plasma cells (PCs) are surrounded by CD163(+) resident macrophages (Mϕs). We show here that human Mϕs (isolated from tonsils or generated from monocytes in vitro) drive activated B cells to differentiate into CD138(+)CD38(++) PCs through secreted CXCL10/IP-10 and VCAM-1 contact. IP-10 production by Mϕs is induced by B cell–derived IL-6 and depends on STAT3 phosphorylation. Furthermore, IP-10 amplifies the production of IL-6 by B cells, which sustains the STAT3 signals that lead to PC differentiation. IP-10–deficient mice challenged with NP-Ficoll show a decreased frequency of NP-specific PCs and lower titers of antibodies. Thus, our results reveal a novel dialog between Mϕs and B cells, in which IP-10 acts as a PC differentiation factor.