jueves, 8 de agosto de 2019

Increased circulating Tfh to Tfr ratio in chronic renal allograft dysfunction: a pilot study | BMC Immunology | Full Text

Increased circulating Tfh to Tfr ratio in chronic renal allograft dysfunction: a pilot study | BMC Immunology | Full Text

BMC Immunology



Increased circulating Tfh to Tfr ratio in chronic renal allograft dysfunction: a pilot study

Abstract

Background

T 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.

Methods

To 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.

Results

The 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).

Conclusion

The imbalance between cTfh and cTfr cells contribute to the development of CAD.

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