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Abstract Number: 14

Abnormalities in Th1, Th2 and Th17 Lymphoid Subpopulations in Long-Term Evolution Primary Antiphospholipid Syndrome

Gabriela Medina1, Oscar I Florez-Durante2, Laura Arcelia Montiel Cervantes3, Rubiraida Molina Aguilar2, Elba Reyes Maldonado2 and Luis J. Jara4, 1Clinical Research Unit, Hospital de Especialidades Centro Medico La Raza,IMSS, Mexico City, Mexico, 2Escuela Nacional de Ciencias Biológicas, Instituto Politécnico Nacional, Mexico City, Mexico, 3Hematology Laboratory, Hospital de Especialidades Centro Médico La Raza, IMSS, Mexico City, Mexico, 4Direction of Education and Research, Hospital de Especialidades Centro Médico La Raza, IMSS, Mexico City, Mexico

Meeting: 2017 ACR/ARHP Annual Meeting

Date of first publication: September 18, 2017

Keywords: antiphospholipid syndrome

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Session Information

Date: Sunday, November 5, 2017

Title: Antiphospholipid Syndrome Poster

Session Type: ACR Poster Session A

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

Background/Purpose: Primary antiphospholipid antibody syndrome (PAPS) is characterized by recurrent thrombosis and pregnancy morbidity in the presence of antiphospholipid antibodies (aPL). Lymphoid subpopulations and innate and adaptive immune responses have not been fully studied in long-term evolution PAPS.

OBJECTIVE: To analyze the lymphoid subpopulations, Th1, Th2 and Th17 immune response in long-term evolution PAPS patients.

Methods: Patients with PAPS >18 years of age, of both genders and a group of healthy blood donors matched for age and sex were included. All patients were receiving oral anticoagulants (Coumadin type). No patient had a recent episode (six months) of thrombosis or other manifestation of APS at the time of the study. Peripheral blood was obtained and lymphoid subpopulations were determined by flow cytometry in order to identify with specific immunological markers, for Treg cells we used: CD4+/CD25+/FoxP3+ and CD8+/CD25+/FoxP3+. The dendritic cells analyzed were: type 1: Lin1-/HLA-DR+/CD11c+; Type 2: Lin1-/HLA-DR+/CD123+; B lymphocytes with CD19+; Monocytes with CD14+; NK: CD3-/CD16+/56+ and NKT: CD3+/CD16+/56+ lymphocytes. Th1 cells were identified by IFN-g+ positivity; Th2: positivity for IL-4+; Th17: positivity for IL-17+. Parametric statistics and Mann-Whitney U-test were used.

Results:

A total of 50 patients with PAPS were included, age: 51.9 ± 12.8, evolution time: 12.8 ± 8.9 years and 35 healthy controls. In patients with PAPS there was a decrease in the total CD3 (p<0.001), CD4 (p<0.005) CD8 (p <0.05) count, Monocytes (p<0.03) B lymphocites (p<0.002), iNKT (p <0.001), DC1 (p <0.001) and DC2 (p <0.001) count cells compared to the control group (Table 1). We found significant decrease in Th1, Th2 and Th17 cytokines basal and after activation compared to healthy controls.

Patients N=50

Controls N=35

p

Median

Median

CD3/uL

962

1351

0.001

CD4/uL

587

786

0.005

CD8/uL

246

445

0.001

nk/uL

129

249

0.02

nkt/uL

33

58

0.02

14/uL (Monocytes)

140

241

0.03

19/uL (B Lymphocites)

41

104

0.002

Tgd/uL

29

45

0.3

iNKT/uL

8

20

0.001

DC1/uL

2

5

0.001

DC2/uL

1

5

0.001

Treg CD4/uL

17

13

0.5

Treg CD8/uL

11

13

0.5

Mann Whitney U test

Conclusion:

This study shows profound alterations in innate and adaptive immunity in patients with long-term PAPS, characterized by a decrease in lymphocyte subpopulations and Th1, Th2, and Th17 cytokines with a possible prevalence of other proinflammatory cytokines and inflammasomes. These abnormalities can become new therapeutic targets in order to restore immune imbalance. Our findings may explain in part, the development of thrombosis, accelerate atherosclerosis and other complications, in PAPS patients with long term disease evolution.


Disclosure: G. Medina, None; O. I. Florez-Durante, None; L. A. Montiel Cervantes, None; R. Molina Aguilar, None; E. Reyes Maldonado, None; L. J. Jara, None.

To cite this abstract in AMA style:

Medina G, Florez-Durante OI, Montiel Cervantes LA, Molina Aguilar R, Reyes Maldonado E, Jara LJ. Abnormalities in Th1, Th2 and Th17 Lymphoid Subpopulations in Long-Term Evolution Primary Antiphospholipid Syndrome [abstract]. Arthritis Rheumatol. 2017; 69 (suppl 10). https://acrabstracts.org/abstract/abnormalities-in-th1-th2-and-th17-lymphoid-subpopulations-in-long-term-evolution-primary-antiphospholipid-syndrome/. Accessed .
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