BAFF-secreting neutrophils drive plasma cell responses during emergency granulopoiesis

J Exp Med. 2016 Jul 25;213(8):1537-53. doi: 10.1084/jem.20150577. Epub 2016 Jul 18.


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.

MeSH terms

  • Animals
  • Antibody Formation / physiology*
  • B-Cell Activating Factor / genetics
  • B-Cell Activating Factor / immunology
  • B-Cell Activating Factor / metabolism*
  • Immunity, Humoral / physiology*
  • Interleukin-17 / genetics
  • Interleukin-17 / immunology
  • Interleukin-17 / metabolism
  • Mice
  • Mice, Knockout
  • Myelopoiesis / physiology*
  • Neutropenia / genetics
  • Neutropenia / immunology
  • Neutropenia / metabolism
  • Neutrophils / cytology
  • Neutrophils / immunology
  • Neutrophils / metabolism*
  • Plasma Cells / immunology
  • Plasma Cells / metabolism*


  • B-Cell Activating Factor
  • Interleukin-17
  • Tnfsf13b protein, mouse