title: Increased circulating follicular helper T cells with decreased programmed death-1 in chronic renal allograft rejection.
abstract: BACKGROUND
  Chronic antibody-mediated rejection is a major issue that affects long-term renal allograft survival. Since follicular helper T (Tfh) cells promote the development of antigen-specific B cells in alloimmune responses, we investigated the potential roles of Tfh cells, B cells and their alloimmune-regulating molecules in the pathogenesis of chronic renal allograft rejection in this study.
  
  
  METHODS
  The frequency of Tfh, B cells and the levels of their alloimmune-regulating molecules including chemokine receptor type 5 (CXCR5), inducible T cell co-stimulator (ICOS), programmed death-1 (PD-1), ICOSL, PDL-1 and interleukin-21 (IL-21), of peripheral blood were comparatively measured in 42 primary renal allograft recipients within 1-3 years after transplantation. Among them, 24 patients had definite chronic rejection, while other 18 patients had normal renal function.
  
  
  RESULTS
  Tfh-cell ratio was significantly increased with PD-1 down-regulation in the patients with chronic renal allograft rejection, while B cells and the alloimmune-regulating molecules studied did not show any appreciable change in parallel.
  
  
  CONCLUSIONS
  The patients with chronic renal allograft rejection have a characteristic increase in circulating Tfh cells with a decrease in PD-1 expression. These pathological changes may be a therapeutic target for the treatment of chronic renal allograft rejection and can be useful as a clinical index for monitoring conditions of renal transplant.
authors.affiliation: Third Clinical College of Soochow University, Changzhou, Jiangsu, China. shijian201205@163.com.
authors.forename: Jian
authors.initials: J
authors.lastname: Shi
authors.affiliation: Third Clinical College of Soochow University, Changzhou, Jiangsu, China. luofengbao@sohu.com.
authors.forename: Fengbao
authors.initials: F
authors.lastname: Luo
authors.affiliation: Third Clinical College of Soochow University, Changzhou, Jiangsu, China. dyqianqian@126.com.
authors.forename: Qianqian
authors.initials: Q
authors.lastname: Shi
authors.affiliation: Third Clinical College of Soochow University, Changzhou, Jiangsu, China. xianlinxu@126.com.
authors.forename: Xianlin
authors.initials: X
authors.lastname: Xu
authors.affiliation: Third Clinical College of Soochow University, Changzhou, Jiangsu, China. czyyhxz@sina.cn.
authors.forename: Xiaozhou
authors.initials: X
authors.lastname: He
authors.affiliation: The University of Texas Medical School at Houston, Houston, TX, USA. Ying.Xia@uth.tmc.edu.
authors.forename: Ying
authors.initials: Y
authors.lastname: Xia
mesh_terms: D000328:Adult; D064591:Allografts / Q000276:immunology / Q000637:transplantation; D001402:B-Lymphocytes / Q000276:immunology*; D002908:Chronic Disease; D005260:Female; D006084:Graft Rejection / Q000209:etiology / Q000276:immunology* / Q000473:pathology*; D006801:Humans; D016030:Kidney Transplantation / Q000009:adverse effects*; D008297:Male; D008875:Middle Aged; D061026:Programmed Cell Death 1 Receptor / Q000276:immunology*; D006377:T-Lymphocytes, Helper-Inducer / Q000276:immunology*; D016896:Treatment Outcome
chemical_list: C105992:PDCD1 protein, human; D061026:Programmed Cell Death 1 Receptor