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Abstract Number: 1858

Investigating The Role Of IL-22 In The Pathogenesis Of Familial Mediterranean FEVER

Dilek Keskin1, Goksal Keskin2, Ali Inal3 and Lale Ozisik4, 1Immunology, DYB Research and Training Hospital, Ankara, Turkey, 2Internal Medicine and Clinical Immunology, DYB Research and Training Hospital, Ankara, Turkey, 3GATA, Immunology, MD, Ankara, Turkey, 4Internal Medicine, MD, Ankara, Turkey

Meeting: 2013 ACR/ARHP Annual Meeting

Keywords: Familial Mediterranean fever

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Session Information

Title: Cytokines, Mediators, Cell-cell Adhesion, Cell Trafficking and Angiogenesis II

Session Type: Abstract Submissions (ACR)

Background/Purpose:

Familial mediterranean fever (FMF) is a familial disease characterized by recurrent episodes of febrile serositis, peritonitis, arthritis andpleuritis. Many studies have been performed as an attempt to understand the basis of the inflammatory attacts in FMF.  During the acute attacts, neutrophil accumulation, elevations in acute phase reactant levels, several non specific immunological abnormalities and increased several proinflammatory cytokines, such as IL-1, IL-8, IL-6 and TNF-alpha have been described.

Th 17 cells are a new class of T-cells involved in a wide range of inflammatory disease. Th17 cells are characterized by production of IL-22 and are known to be key participants in various inflammatory disease, such as, BD, crohn’disease, sarcoidosis.  IL-22 acts synergistically with TNF alpha, IL-1 beta or IL-17 and induces acute phase reactants.  These findings indicate that IL-22 represents a novel type of immune mediator that is produced by immune cells which regulates tissue protection and homeostasis.  So the aim of this study was to investigate the role of serum IL-22 levels in patients with FMF.

Methods: Fifty-seven patients with FMF and 18 healthy controls (8 female, 10 male; mean age 33.7 ± 2.9 years) were enrolled in this study.  Thirty-nine patients were in active stage (17 female, 22 male, mean age; 31.7 ± 3.1 years, mean disease duration 6.3 ± 2.8 years) and 18 patients were in inactive stage (9 female,9 male, mean age; 34.7 ± 4.9 years, mean disease duration; 8.1 ± 4.3 years).  Serum IL-22 levels were determined by ELISA.

Results:

In active patients, the mean ESR was 41.9 ± 8.2 mm/h, the mean serum CRP level was 28.6 ± 6.8 mg/L and the mean serum fibrinogen level was 514.3 ± 88.3 mg/dl.            In inactive patients, the mean ESR was 18.3 ± 4.7 mm/h, the mean serum CRP level was 2.4 ± 1.6 mg/L and the mean serum fibrinogen level was 197.3 ± 62.9 mg/dl.              The mean serum IL-22 levels were 56.4 ± 8.5 pg/ml in patients with FMF and  21.7 ± 3.9 pg/ml in healthy controls.  The mean serum IL-22 levels were 73.5 ± 7.9 pg/ml in active patients and 38.2 ± 8.3 pg/ml in inactive patients. 

            According to this result; serum IL-22 levels were significantly high in patients with FMF compared to healthy controls (p<0.001).  Serum IL-22 levels were significantly high in active patients  compared to inactive patients and healthy controls (p<0.001 and p<0.001 respectively). 

In active FMF patients, although the mean serum IL-22 level was correlated with the mean serum fibrinogen level (r=0.508 p=0.027) and serum CRP level (r=0.482, p=0.039), the mean serum IL-22 level was not correlated with ESR (r=0.334, p=0.085).

Conclusion: The high levels of serum IL-22, in active and inactive patients with FMF suggest that IL-22 may play a significant role of in the pathogenesis of FMF. 


Disclosure:

D. Keskin,
None;

G. Keskin,
None;

A. Inal,
None;

L. Ozisik,
None.

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