Repetitive ischemic injuries to the kidneys result in lymph node fibrosis and impaired healing

• DOI: 10.1172/jci.insight.120546
• Publication Date: 2018-07-11T15:01:22Z
• Authors: Omar H. Maarouf; Mayuko Uehara; Vivek Kasinath; Zhabiz Solhjou; Naima Banouni; Baharak Bahmani; Liwei Jiang; Osman A. Yilmam; Indira Guleria; Scott B. Lovitch; Jane L. Grogan; Paolo Fiorina; Peter T. Sage; Jonathan S. Bromberg; Martina M. McGrath; Reza Abdi
• Keywords: Homeodomain Proteins; Male; Mice, Knockout; 0301 basic medicine; Immunoglobulins; Acute Kidney Injury; Kidney; Fibrosis; 3. Good health; Mice, Inbred C57BL; Disease Models, Animal; Mice; 03 medical and health sciences; Chronic kidney disease; Fibrosis; Nephrology; Lymphotoxin beta Receptor; Reperfusion Injury; Animals; Lymph Nodes; Signal Transduction

The contribution of the kidney-draining lymph node (KLN) to pathogenesis ischemia-reperfusion injury (IRI) kidney and its subsequent recovery has not been explored in depth. In addition, mechanism by which repetitive IRI contributes renal fibrosis remains poorly understood. Herein, we have found that is associated with expansion high endothelial venules (HEVs) activation fibroblastic reticular cells (FRCs) KLN, as demonstrated significant extracellular matrix. lymphotoxin α signaling pathway mediates FRCs, chronic treatment β receptor-immunoglobulin fusion protein (LTβr-Ig) resulted marked alteration KLN well augmentation fibrosis. Depletion FRCs reduced T cell ameliorated acute IRI. Repetitive was senescence scarring, were FRC administration. Therefore, our study emphasizes critical role both initiation repair phases following kidney.