Abstract
BackgroundT follicular helper (Tfh) cells play a control role in contribution of B cell differentiation and antibody production. T follicular regulatory (Tfr) cells inhibit Tfh-B cell interaction.MethodsTo identify whether circulating Tfh (cTfh) and Tfr (cTfr) cells contribute to chronic renal allograft dysfunction (CAD), 67 kidney transplant recipients (34 recipients with CAD, 33 recipients with stable function) were enrolled. The frequency of cTfh and cTfr cells, the level of serum CXCL13 were measured.ResultsThe frequency of cTfr cells in CAD group was significantly lower than that in stable group (0.31% vs 0.68%, P = 0.002). The cTfh to cTfr ratio in CAD group was significantly higher than that in stable group (55.4 vs 25.3, P = 0.013). Serum CXCL13 in CAD group was significantly higher than stable group (30.4 vs 21.9 ng/ml, P = 0.025). After linear regression analysis, the cTfh to cTfr ratio was an independent risk factor for estimated glomerular filtration rate (eGFR) in recipients (standardized coefficient = − 0.420, P = 0.012). After logistic regression analysis, the cTfh to cTfr ratio was an independent risk factor for CAD (OR = 1.043, 95%CI = 1.004–1.085, P = 0.031).ConclusionThe imbalance between cTfh and cTfr cells contribute to the development of CAD.
Highlights
T follicular helper (Tfh) cells play a control role in contribution of B cell differentiation and antibody production
In the present study, we found that the frequency of C-X-C chemokine receptor 5 (CXCR5)+ on CD4+ cells and circulating T follicular regulatory (Tfr) (cTfr) cells were decreased in chronic renal allograft dysfunction (CAD) group than stable group
We found that the circulating Tfh (cTfh) to cTfr ratio was significantly higher in recipients with antibody-mediated rejection (ABMR) or Donor-specific antibodies (DSA) than recipients with stable renal function
Summary
T follicular helper (Tfh) cells play a control role in contribution of B cell differentiation and antibody production. The risk of acute rejection after kidney transplantation has been decreased with the development of immunosuppressant and transplant technique, while chronic renal allograft dysfunction (CAD) is still the main threat for long-term allograft survival rates. Antibody-mediated injury or rejection is the leading cause of late kidney allograft dysfunction [1, 2]. Donor-specific antibodies (DSA) could identify patients at high risk for kidney allograft loss [3, 4]. Avoiding the influence of humoral immune factors on allograft function could decline the risk of CAD. The production of high affinity antibody in germinal center (GC) requires the help of T follicular helper (Tfh) cells [5]. Tfh cells in lymph node highly express C-X-C chemokine receptor 5 (CXCR5), programmed death 1
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