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AB0126 Autophagy and systemic lupus erythematosus: clinical significance of ATG14+, FOXP3+, and CD25+ expression on T regulatory cells and nk cells
  1. A Rodríguez1,
  2. EJ Zurita1,
  3. AR Durán2,
  4. R Bustamante3,
  5. A Sánchez3,
  6. MΆ Saavedra3,
  7. C Arroyo4,
  8. G Medina5,
  9. LJ Jara3
  1. 1Immunology Department, Escuela Nacional de Ciencias Biologicas
  2. 2Immunology Department, Escuela Nacional de Ciencias Biolόgicas
  3. 3Rheumatology Department
  4. 4Banco de Sangre, Hospital de Especialidades “Dr. Antonio Fraga Mouret”, Centro Médico la Raza, IMSS
  5. 5Rheumatology Department, Hospital de Especialidades “Dr. Antonio Fraga Mouret”, CENTRO, Mexico City, Mexico

Abstract

Background Autophagy is a highly conserved protein degradation pathway, essential for removing protein aggregates and misfolded proteins in healthy cells. Autophagy and autophagy-molecules expression have been implicated in autoimmune diseases. Systemic Lupus Erythematosus (SLE) is a prototype of autoimmune disease whose main characteristic is the loss of immune tolerance. Recent evidences suggest that autophagy, and autophagy-related proteins participate in SLE immune regulation. However, little is known about the SLE clinical significance of autophagy-related proteins, T regulatory, and NK cells.

Objectives To evaluate the expression of ATG14+ (autophagy-related key regulator protein), FOXP3+, CD25+T regulators, CD56+NK cells in active and inactive SLE patients.

Methods The expression of ATG14+, FOXP3+, CD25+, and CD56+ were measured by flow cytometry, and expressed in percentages in T and NK cells of SLE patients (1997, ACR criteria), and healthy controls. Active SLE was considered by SLEDAI (≥4). The organs affected and treatments were evaluated.

Results A total of 40 SLE patients and 20 healthy controls were included. The mean expression of autophagy in 20 active SLE patients was 11.19% in comparison with inactive SLE patients, 7.13%, (p=0.04), and in healthy donors, 7.445% (p=0.0281). The FOXP3+ expression in NK cells in active SLE was lower in comparison with inactive patients (0.98% vs 3.82% respectively). In healthy donors was 2.89%.

Conclusions We found that in active patients autophagy is higher than in inactive patients. In inactive patients FOXP3 expression in NK cells is normal. These results can be due to the effect of the different treatments given according to clinical manifestations. Autophagy-related key regulator protein may be a new target of SLE treatment

References

  1. Lech M, Anders HJ. The pathogenesis of lupus nephritis. J Am Soc Nephrol. 2013, 24, 1357–1366.

  2. Chikte S, et. al. use of LysoTracker dyes: A flow cytometric study of autophagy. Cytometry. 2014, 85(2), 169–78.

References

Disclosure of Interest None declared

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