English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Zendy Plus

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Zendy Tools

Zendy Open

Renal fibrosis is a significant threat to public health globally. Diverse primary aetiologies eventually result in chronic kidney disease ( CKD ) and immune cells influence this process. The roles of monocytes/macrophages, T cells, and mast cells have been carefully examined, whilst only a few studies have focused on the effect of B cells. We investigated B‐cell function in tubulointerstitial fibrosis induced by unilateral ureteral obstruction ( UUO ), using genetic B‐cell‐deficient  μMT  mice or  CD20  antibody‐mediated B‐cell‐depleted mice. Obstructed kidneys of  μMT  and anti‐ CD20 ‐treated mice showed lower levels of monocyte/macrophage infiltration and collagen deposition compared to wild‐type mice. Mechanistically, anti‐ CD20  attenuated  UUO ‐induced alterations of renal tumour necrosis factor‐α ( TNF ‐α), vascular cell adhesion molecule 1 ( VCAM ‐1) pro‐inflammatory genes, and  CC  chemokine ligand‐2 ( CCL2 ) essential for monocyte recruitment; B cells were one of the main sources of  CCL2  in post‐ UUO  kidneys. Neutralization of  CCL2  reduced monocyte/macrophage influx and fibrotic changes in obstructed kidneys. Therefore, early‐stage accumulation of B cells in the kidney accelerated monocyte/macrophage mobilization and infiltration, aggravating the fibrosis resulting from acutely induced kidney nephropathy. © 2016 The Authors. Journal of Pathology published by John Wiley & Sons Ltd on behalf of Pathological Society of Great Britain and Ireland.

the journal of pathology

Renal recruitment of B lymphocytes exacerbates tubulointerstitial fibrosis by promoting monocyte mobilization and infiltration after unilateral ureteral obstruction