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BAFF-secreting neutrophils drive plasma cell responses during emergency granulopoiesis

Prolonged infections or adjuvant usage can trigger emergency granulopoiesis (EG), leading to dysregulation in neutrophil blood counts. However, the impact of EG on T and B cell function remains largely unknown. In this study, to address this question, we used a mouse model of neutropenia and studied...

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Detalles Bibliográficos
Autores principales: Parsa, Roham, Lund, Harald, Georgoudaki, Anna-Maria, Zhang, Xing-Mei, Ortlieb Guerreiro-Cacais, André, Grommisch, David, Warnecke, Andreas, Croxford, Andrew L., Jagodic, Maja, Becher, Burkhard, Karlsson, Mikael C.I., Harris, Robert A.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Rockefeller University Press 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4986521/
https://www.ncbi.nlm.nih.gov/pubmed/27432941
http://dx.doi.org/10.1084/jem.20150577
Descripción
Sumario:Prolonged infections or adjuvant usage can trigger emergency granulopoiesis (EG), leading to dysregulation in neutrophil blood counts. However, the impact of EG on T and B cell function remains largely unknown. In this study, to address this question, we used a mouse model of neutropenia and studied immune activation after adjuvant administration. The initial neutropenic state fostered an environment of increased dendritic cell activation and T cell–derived IL-17 production. Interestingly, neutropenic lysozyme 2–diphtheria toxin A mice exhibited striking EG and amplified neutrophil recruitment to the lymph nodes (LNs) that was dependent on IL-17–induced prostaglandin activity. The recruited neutrophils secreted a B cell–activating factor that highly accelerated plasma cell generation and antigen-specific antibody production. Reduction of neutrophil functions via granulocyte colony-stimulating factor neutralization significantly diminished plasma cell formation, directly linking EG with the humoral immune response. We conclude that neutrophils are capable of directly regulating T cell–dependent B cell responses in the LN.