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AB0017 Hla-g 3′utr 14bp polymorphism and shla-g levels in tunisian patients with behçet’s disease
  1. M. Maatouk1,
  2. K. Sakly1,
  3. S. Hammami2,
  4. M. Boufaroua1,
  5. F. Nefzi3,
  6. T. Trimeche4,
  7. O. Harzallah2,
  8. S. Mahjoub2,
  9. I. Ghedira1,
  10. S. Feki1,
  11. N. Sakly1,5
  1. 1Research unit 03/UR/07 “autoimmunity and allergy”, Faculty of pharmacy
  2. 2Internal medicine, Fattouma Bourguiba University Hospital
  3. 3Laboratory of Transmissible Diseases and Biological Active Substances, LR99ES27, Faculty of Pharmacy
  4. 4Laboratory of Biochemical, faculty of medicine
  5. 5Laboratory of Microbiology, Unity of Immunology of EPS Fattouma Bourguiba, Monastir, Tunisia

Abstract

Background Behcet’s disease (BD) is a chronic relapsing multisystemic inflammatory disease. Although the actual etiology is still unclear, BD symptoms are considered to be the resultant of genetic intrinsic factors and triggering extrinsic factors [1]. HLA-G is a non-classical HLA-class I molecule and has multiple immunoregulatory properties. A 14 bp insertion/deletion polymorphism in the HLA-G gene has been suggested to influence the level of soluble HLA-G and then to associate with certain pathological conditions, including inflammatory diseases [2].

Objectives The aim of this study was to investigate the HLA-G 3′UTR 14bp polymorphism and sHLA-G levels in Tunisian patients with BD.

Methods 120 patients with BD, 77 males and 43 females (mean age: 38.13±11.7 years), were recruited from the internal medicine department at Fattouma Bourguiba Hospital of Monastir in Central region of Tunisia. 168 volunteer donors were recruited as healthy controls (HC) (mean age: 30.41± 9.05 years). HLA-G 14bp deletion/insertion polymorphism was detected by PCR amplification of the target sequence followed by agarose gel electrophoresis. Serum levels of soluble HLA-G (sHLA-G) were measured for 49 patients with BD (34 inactive cases, 15 active cases) and 49 healthy controls using a commercial ELISA kit.

Results A significant decreased frequency of the +14bp HLA-G allele was detected in patients with BD compared to HC (0.36 vs 0.77, P = 0.036). A significant increased frequency of HLA-G -14/-14bp was observed in patients with BD compared to HC [0.36 vs 0.22, P = 0.022, OR 0.52 (95% CI 0.29–0.93)]. The median plasmatic concentration of sHLA-G was higher in patients with BD compared to HC without significant difference (96.4 (56.4-150.65) vs 65.1 (47-136.9) U/ml, P=0.1]. However, sHLA-G levels were significantly increased in patients with active disease [150.3 (91.4-265) U/ml] compared to patients with inactive disease [85.7 (55-1127.9) U/ml, P=0.038] and HC (P=0.044). Furthermore, our results showed that the 14bp polymorphism was significantly associated with the level of sHLA-G expression. In fact, +14/+14bp subjects had significantly lower plasmatic levels of sHLA-G compared to the group with the +14/-14bp genotype (P = 0.011) or the group of individuals +14/-14bp or -14/-14bp (P = 0.004).

Conclusions The homozygous 14pb insertion is associated with decreased plasmatic levels of sHLA-G in Tunisians. Moreover, homozygous deletions are more frequent in patients with BD compared to controls and sHLA-G levels are higher in patients with active disease, suggesting a possible involvement in the disease physiopathology.

  1. Kaneko, F., et al., Behcet’s disease (Adamantiades-Behcet’s disease). Clin Dev Immunol, 2011. 2011: p. 681956.

  2. Hviid, T.V., et al., HLA-G and IL-10 in serum in relation to HLA-G genotype and polymorphisms. Immunogenetics, 2004. 56(3): p. 135-41.

Disclosure of Interest None Declared

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