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THU0038 Abnormal Phenotypic T Cell Subsets in Peripheral Blood of Tunisian Patients with Behcet’s Disease
  1. K. Sakly1,
  2. C. Lambert2,
  3. M. Maatouk1,
  4. S. Hammami3,
  5. N. Sakly1,4,
  6. O. Harzallah3,
  7. F. Nefzi5,
  8. S. Mahjoub3,
  9. I. Ghedira1,
  10. S. Feki1
  1. 1Research Unit 03/UR/07 “Autoimmunity and Allergy”, Faculty of Pharmacy, Monastir, Tunisia
  2. 2Laboratory of Immunology, University Hospital Saint Etienne, Saint Etienne, France
  3. 3Internal medicine, F.B. University Hospital
  4. 4Unity of Immunology of EPS Fattouma Bourguiba
  5. 5Laboratory of Transmissible Diseases and Biological Active Substances, LR99ES27, Faculty of Pharmacy, Monastir, Tunisia

Abstract

Background Behçet’s disease (BD) is a chronic recurrent multisystemic inflammatory disorder of unknown origin. Immune-mediated mechanisms play a major role in the pathogenesis of the disease. BD is not considered to be an autoimmune disorder, and the character of the disease needs to be clarified [1].

Objectives The aim of this study was to determine the immunophenotypic profile of T cell subsets in patients with BD.

Methods 30 patients with BD, 19 males and 11 females (mean age: 39.65±10.7 years) were enrolled in this study. They are constituted of 20 patients with inactive cases and 10 patients with active cases. Eight volunteer donors were recruited as healthy controls (HC) (mean age: 32.8±13.6 years). The following monoclonal antibody combination was used to characterize the phenotypes of T cells: anti-CD4-Chrome orange/anti-CD3-PacificBlue/anti-CD62L-PE/anti-CD127-APC-Cy7/anti-CD25-PerCP-Cy5/anti-CD45RA-PCy7 and anti-CD8-APC. Analysis was performed on a FACSDiva flow cytometer using FACSDiva™ software.

Results Our study showed that patients with BD, as compared with HC, had significantly decreased percentage of CD25brightCD127- CD4+ Treg cells (3.38 ± 1.7% versus 4.8 ± 0.26%; P = 0.039), significantly reduced percentage of CD45RA+CD62L+CD4+ naïve T cells (8.16 ± 6.34% versus 26.7 ± 6.4%; P = 0.001) and increased percentage of CD45RA–CD62L– CD4+ effector memory T cells (56.41 ± 19.5% versus 32.07 ± 8.5%; P = 0.04). However, no differences were found between patients and HC regarding T CD8+ cell subsets. On the other hand, patients with active BD showed, in comparison to patients in remission, decreased percentages of CD45RA+CD62L+CD4+ naïve T cells (4.19 ± 3.1% versus 11.25 ± 6.42%; P = 0.02) and terminally differentiated CD45RA+CD62L-CD4+ effector memory T cells (9.29 ±3.6% versus 18.97 ± 11.34%; P = 0.013) but increased percentages of CD4+CD45RA-CD62L- effectors memory T cells (70.61± 11.82% versus 48.78 ± 17%; P = 0.005). Moreover, patients with active BD are characterized by significantly decreased CD45RA+CD62L+CD8+ naïve T cells compared to patients in remission (6.49±4% versus 13.87±6.8%; P=0.017) and a significantly increased percentage of CD45RA–CD62L–CD8+ effectors memory T cells (63.89±13.4% versus 44.36±11.9%; P=0.004).

Conclusions Our study showed that patients with BD are characterized by decreased percentages of T regs and increased percentages of effector memory T cells. The latter subset of T cells is also increased in active BD. The understanding of these findings could contribute to the clarification of the role of these cell subsets in the pathogenesis of BD and disease activity.

References

  1. Kapsimali, V.D., et al., Etiopathogenesis of Behcet’s disease with emphasis on the role of immunological aberrations. Clin Rheumatol, 2010. 29(11): p. 1211-6.

Disclosure of Interest None Declared

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