| First Author | Parsa R | Year | 2016 |
| Journal | J Exp Med | Volume | 213 |
| Issue | 8 | Pages | 1537-53 |
| PubMed ID | 27432941 | Mgi Jnum | J:236544 |
| Mgi Id | MGI:5806363 | Doi | 10.1084/jem.20150577 |
| Citation | Parsa R, et al. (2016) BAFF-secreting neutrophils drive plasma cell responses during emergency granulopoiesis. J Exp Med 213(8):1537-53 |
| abstractText | 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. |
