title: CXCL10 and CXCL13 Expression were highly up-regulated in peripheral blood mononuclear cells in acute rejection and poor response to anti-rejection therapy.
abstract: BACKGROUND
  Acute rejection is still one of the main complications which enhances the cost and the risk to renal graft failure. Chemokines, interacting with respective receptors, can recruit leukocytes into grafts and mediate allograft rejection. In this study, we aimed to analyze gene expression of chemokines including CCL5/RANTES, CXCL10/IP-10, CXCL13/BCA-1, and receptors of CCR5, CXCR3, CXCR5 in peripheral blood mononuclear cells (PBMCs) during acute renal allograft rejection
  
  
  METHODS
  Gene expression of all these chemokines and receptors in PBMCs were analyzed by real-time PCR from 14 stable recipients, 32 biopsy-proven acute rejection (AR), and 5 acute tubular necrosis (ATN).
  
  
  RESULTS
  Gene expression of CCL5, CXCL10, CXCL13, and CCR5 were up-regulated both in AR and ATN group compared to stable recipients (fold change>2, P<0.05). Serum creatinine recovered to baseline level after anti-rejection therapy was defined as AR-sensitive and creatinine maintained above 200 μmol/L as AR-resistant. Expression of CXCL10 and CXCL13 were 5.98-, 2.94-, and 20.5, 10.8-fold change in AR-resistant and AR-sensitive compared to stable recipients, respectively. The expression of CXCL10 and CXCL13 was a twofold change in AR-resistant compared to AR-sensitive recipients (P<0.05). Five out of ten AR-resistant recipients lost graft function in the follow-up.
  
  
  CONCLUSIONS
  CXCL10 and CXCL13 expression were highly up-regulated in PBMCs in acute renal allograft rejection, especially in poor response to anti-rejection therapy and detrimental prognosis.
authors.affiliation: Kidney Disease Center, the First Affiliated Hospital of Medical College, Zhejiang University, 79 Qingchun road, Hangzhou, 310003, China.
authors.forename: Youying
authors.initials: Y
authors.lastname: Mao
authors.forename: Minmin
authors.initials: M
authors.lastname: Wang
authors.forename: Qin
authors.initials: Q
authors.lastname: Zhou
authors.forename: Juan
authors.initials: J
authors.lastname: Jin
authors.forename: Yucheng
authors.initials: Y
authors.lastname: Wang
authors.forename: Wenhan
authors.initials: W
authors.lastname: Peng
authors.forename: Jianyong
authors.initials: J
authors.lastname: Wu
authors.forename: Zhangfei
authors.initials: Z
authors.lastname: Shou
authors.forename: Jianghua
authors.initials: J
authors.lastname: Chen
mesh_terms: D000293:Adolescent; D000328:Adult; D001706:Biopsy; D018946:Chemokine CCL5 / Q000097:blood / Q000235:genetics / Q000276:immunology; D054357:Chemokine CXCL10 / Q000097:blood / Q000235:genetics / Q000276:immunology; D054382:Chemokine CXCL13 / Q000097:blood / Q000235:genetics / Q000276:immunology; D015870:Gene Expression; D006084:Graft Rejection / Q000097:blood* / Q000235:genetics / Q000276:immunology; D006801:Humans; D007165:Immunosuppression Therapy / Q000379:methods; D007166:Immunosuppressive Agents / Q000494:pharmacology; D007668:Kidney / Q000276:immunology* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D007673:Kidney Cortex Necrosis / Q000097:blood* / Q000235:genetics / Q000276:immunology; D016030:Kidney Transplantation / Q000276:immunology*; D007963:Leukocytes, Mononuclear; D008875:Middle Aged; D016133:Polymerase Chain Reaction; D012333:RNA, Messenger; D019713:Receptors, CCR5 / Q000097:blood / Q000235:genetics / Q000276:immunology; D054367:Receptors, CXCR3 / Q000097:blood / Q000235:genetics / Q000276:immunology; D054380:Receptors, CXCR5 / Q000097:blood / Q000235:genetics / Q000276:immunology; D012189:Retrospective Studies; D015854:Up-Regulation
chemical_list: C114753:CXCL10 protein, human; C110663:CXCL13 protein, human; C515187:CXCR3 protein, human; C095085:CXCR5 protein, human; D018946:Chemokine CCL5; D054357:Chemokine CXCL10; D054382:Chemokine CXCL13; D007166:Immunosuppressive Agents; D012333:RNA, Messenger; D019713:Receptors, CCR5; D054367:Receptors, CXCR3; D054380:Receptors, CXCR5