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Abstract Number: 781

Simultaneous Identification of Two Biomarkers in ACTIVE LUPUS Nephritis: Autophagy in Treg CELLS and Prolactin Receptors in B Lymphocytes

Luis J. Jara-Quezada1, Emma Zurita2, Ana Durán2, Antonio Sanchez3, Reyna Bustamante3, Gabriela Medina4, Miguel A Saavedra5, María Pilar Cruz-Dominguez3, Olga Vera-Lastra6, María Pilar Jiménez-Arellano7, Michel Augusto Martínez-Bencomo3 and Azucena Rodriguez2, 1Departamento de Inmunología, Escuela Nacional de Ciencias Biológicas, Instituto Politécnico Nacional,, Mexico, Mexico, 2Departamento de Inmunología, Escuela Nacional de Ciencias Biológicas, Instituto Politécnico Nacional,, Mexico City, Mexico, 3Hospital de Especialidades "Dr. Antonio Fraga Mouret", Centro Médico Nacional "La Raza", Mexico City, Mexico, 4Clinical Research Unit, Hospital de Especialidades Centro Medico La Raza,IMSS, Mexico City, Mexico, 5Novartis Farmaceutica, Calz de Tlaplan 1779, Mexico, Mexico, 6Rheumatology, Instituto Mexicano Seguro Social, Mexico City, Mexico, 7Hospital de Especialidades "Dr. Antonio Fraga Mouret", Centro Médico Nacional "La Raza", Mexico CIty, Mexico

Meeting: 2018 ACR/ARHP Annual Meeting

Keywords: autophagy, Biomarkers, lupus nephritis and prolactin, T-Regulatory Cells

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Session Information

Date: Sunday, October 21, 2018

Title: Systemic Lupus Erythematosus – Clinical Poster I: Clinical Manifestations and Comorbidity

Session Type: ACR Poster Session A

Session Time: 9:00AM-11:00AM

Background/Purpose: Recent studies suggest that autophagy defects contributes to systemic lupus erythematosus (SLE) pathogenesis. Prolactin (PRL) is associated with active SLE and stimulates the immune cells by binding to receptor (PRL-R). Prolactin decreases the suppressor function exerted by Treg cells favoring an inflammatory microenvironment in SLE. The objective is simultaneously identify the expression of autophagy in Treg lymphocytes and PRL-R in B lymphocytes of SLE patients.

Methods: We included 40 patients with SLE (ACR criteria) divided into two groups: Group 1: patients with remission SLE (SLEDAI <4), Group 2: patients with active SLE (SLEDAI > 4). The affected organs and the treatments received were obtained. As a control group, we included  healthy individuals. A fasting peripheral blood sample was taken from all patients and controls. The cells were separated and labeled with specific antibodies: Treg cells: CD25+, FoxP3+, Atg14+ (autophagy marker), and B lymphocytes: CD19+, PRL-R+. Analysis was performed by flow cytometry. ANOVA test was used for statistical analysis.

Results: We included 40 patients, divided in 20 inactive, 20 active SLE patients and 20 healthy controls. 80% of our population were female. Evolution time in inactive SLE patients was 8.72±1.16 years and in active SLE patients was 5±0.95 years. SLEDAI was higher in active SLE patients than inactive SLE patients. In both active and inactive SLE groups, kidney was the most affected major organ (55% and 25% respectively). Sixty percent of inactive SLE patients and 35% of active patients had Chloroquine. The expression of autophagy, Treg cells Prolactin receptors and B-lymphocytes are shown in Figures 1 and 2.

Conclusion: The increase of autophagy in Treg and PRL-R in B lymphocytes participate in active lupus glomerulonephritis. Autophagy and PRL-R may be new therapeutic targets in SLE.This results suggest that may be a connection between autophagy, PRL-R, Treg and B cells if any.

Fig.1: A) Dot plot in logarithmic scale of peripheral blood mononuclear cells (PBMC) of a SLE patient. B) Dot plot of the percentage of CD4 + CD25 + expression for Treg lymphocytes. C) Dot plot of the percentage of CD4 + CD25 + expression for Treg lymphocytes

 

Fig. 2: Left: autophagy (%) in Treg cells in patients  and controls: A: Healthy control vs. Inactive SLE: 7.44 vs 8.74   p= >0.9999 B: Healthy control vs. Active SLE: 7.44 vs 12.11    p= <0.05. Right: prolactin Receptor in B lymphocytes, in Active and Inactive patients and healthy controls: A: Healthy Controls vs Inactive SLE: 0.62 vs 3.56 p= 0.7463. B: Heatlhy Controls vs Active SLE: 0.62 vs 50.79 p= <0.0001


Disclosure: L. J. Jara-Quezada, None; E. Zurita, None; A. Durán, None; A. Sanchez, None; R. Bustamante, None; G. Medina, None; M. A. Saavedra, None; M. P. Cruz-Dominguez, None; O. Vera-Lastra, None; M. P. Jiménez-Arellano, None; M. A. Martínez-Bencomo, None; A. Rodriguez, None.

To cite this abstract in AMA style:

Jara-Quezada LJ, Zurita E, Durán A, Sanchez A, Bustamante R, Medina G, Saavedra MA, Cruz-Dominguez MP, Vera-Lastra O, Jiménez-Arellano MP, Martínez-Bencomo MA, Rodriguez A. Simultaneous Identification of Two Biomarkers in ACTIVE LUPUS Nephritis: Autophagy in Treg CELLS and Prolactin Receptors in B Lymphocytes [abstract]. Arthritis Rheumatol. 2018; 70 (suppl 9). https://acrabstracts.org/abstract/simultaneous-identification-of-two-biomarkers-in-active-lupus-nephritis-autophagy-in-treg-cells-and-prolactin-receptors-in-b-lymphocytes/. Accessed .
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