• 2018-07
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  • 2019-04
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  • 2020-01
  • EBI is known to play a critical role in


    EBI2 is known to play a critical role in the induction of antibody responses in secondary lymphoid tissues.13, 14 However, little is known about the expression and function of EBI2 in human peripheral tissues. To our knowledge, this is the first report of increased EBI2 levels in peripheral tissues of a human pathological condition. We have found a significant increase in both EBI2 gene and protein expression in NPs in this study (Fig 5). Given the known role of EBI2 in facilitating plasmablast development and antibody production, and the striking enhancement of local production of CNQX in NPs, it is reasonable to speculate that EBI2 expression could be playing a role in this process in NPs. In addition, this work highlights EBI2 as a potential new therapeutic target that warrants further investigation. We have also shown that EBI2 levels correlate with markers of plasma cells in patients with CRS, lending further support to a potential role in disease pathogenesis, although future studies are needed to confirm whether EBI2 plays a role in activating local plasma cell responses in patients with CRS. The present studies suggest a potential importance of EBI2 expression in peripheral tissues in human subjects and extend our knowledge of the local mechanisms that promote B cells, plasma cells, and immunoglobulins in patients with CRSwNP-induced inflammation. In summary, we have shown that NPs from patients with CRS had abundant accumulation of inflammatory cells, especially B cells and plasma cells. Not surprisingly, we also found significantly increased levels of several antibody isotypes in NPs. Finally, we have shown that EBI2 was highly expressed in NPs and correlated with expression of plasma cell markers. These findings indicate that B-cell inflammatory responses occur locally in NPs, might play a critical role in the pathogenesis of CRSwNP, and might provide novel insights for the development of improved therapeutic interventions.