4.2 Article

Alloantigen-stimulated induction and release of CD30 in patients with end-stage renal failure

Journal

HUMAN IMMUNOLOGY
Volume 73, Issue 11, Pages 1102-1108

Publisher

ELSEVIER SCIENCE INC
DOI: 10.1016/j.humimm.2012.08.015

Keywords

-

Categories

Funding

  1. Talented Young Women Award, Alcaldia de Medellin, Medellin, Colombia
  2. Colciencias, Bogota, Colombia
  3. Secretaria de las Mujeres, Alcaldia de Medellin, Medellin, Colombia
  4. Estrategia de Sostenibilidad, Vicerrectoria de Investigacion, Universidad de Antioquia

Ask authors/readers for more resources

High serum levels of soluble CD30 (sCD30) are associated with poor renal allograft survival, and regulatory T cells (Tregs) influence allograft survival depending on CD30 signaling. However, how 5CD30 modulates alloimmune responses remains poorly understood. We measured the level of Tregs and sCD30 in patients with end-stage renal failure (ESRF) and analyzed whether allo- or polyclonal stimulation of the patients' T cells results in the expression and release of CD30. ESRF patients showed increased serum 5CD30 levels and lower percentages of circulating Tregs as compared to healthy controls (HC) (p < 0.001 and 0.024). Polyclonal and allogeneic stimulation resulted in higher expression of CD30, and after polyclonal stimulation, ESRF patients showed higher percentages of CD30-expressing T cells than HC (p < 0.001). Compared to autologous stimulation, allogeneic stimulation induced significantly higher expression of CD30 on T cells of ESRF patients only. After polyclonal as well as allogeneic stimulation, an increased sCD30 content was found in culture supernatants of both ESRF patients and HC (p <0.001). Together with decreased Tregs, high serum sCD30 and increased induction of CD30 on T cells after polyclonal stimulation may explain exacerbated alloimmune responses and poor allograft survival in ESRF patients in whom immunosuppression is not able to control the alloimmune response. (C) 2012 American Society for Histocompatibility and Immunogenetics. Published by Elsevier Inc. All rights reserved.

Authors

I am an author on this paper
Click your name to claim this paper and add it to your profile.

Reviews

Primary Rating

4.2
Not enough ratings

Secondary Ratings

Novelty
-
Significance
-
Scientific rigor
-
Rate this paper

Recommended

No Data Available
No Data Available