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• Soluble TRAIL concentrations are raised in patients with systemic lupus erythematosus
  Gabriella Castellino
  Published on: 25 August 2005

• Published on: 25 August 2005

  Soluble TRAIL concentrations are raised in patients with systemic lupus erythematosus

  • Gabriella Castellino, MD
  • Other Contributors:
    • Francesco Trotta, *Federica Corallini, *Paola Secchiero

  Dear Editor,

  In their report on concentrations of TNF related apoptosis inducing ligand (TRAIL) in Systemic Lupus Erythematosus (SLE) patients, Lub-de Hooge et al stated that, notwithstanding SLE activity, TRAIL is increased in the serum of SLE patients compared to patients affected from Rheumatoid Arthritis (RA), Wegener’s granulomatosis and healthy subjects. Their study followed previous observations related to in...

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  Dear Editor,

  In their report on concentrations of TNF related apoptosis inducing ligand (TRAIL) in Systemic Lupus Erythematosus (SLE) patients, Lub-de Hooge et al stated that, notwithstanding SLE activity, TRAIL is increased in the serum of SLE patients compared to patients affected from Rheumatoid Arthritis (RA), Wegener’s granulomatosis and healthy subjects. Their study followed previous observations related to increased expression of TRAIL, both in membrane-bound and soluble form, in SLE patients with neutropenia.[1,2] The authors concluded that increased sTRAIL levels may amplify the abnormal apoptotic process in SLE responsible for accumulation of apoptotic cells in the peripheral blood and induction of autoimmunity and suggested that increased sTRAIL levels is disease specific for SLE. Even if this hypothesis is very intriguing, a similar study conducted in our centre proved different results.

  Through ELISA we have measured sTRAIL concentration in 40 SLE patients (10 with active and 30 with inactive disease treated with a constant dose of an immunomodulating agent), 35 RA patients and a group of healthy subjects. We have found sTRAIL levels comparable in the 3 groups and respectively of 76 pg/ml (SD ± 34), 98 pg/ml (SD ± 43) and 75 pg/ml (SD ± 23). In accordance with authors’ data we didn’t found any correlation between sTRAIL levels and any specific manifestation of the disease or with SLE disease activity index. In particular, we didn’t found any correlation between TRAIL levels and blood cell counts (neutropenia).

  Even if the hypothesis of an increased apoptosis as a mechanism of SLE inducing autoimmune response is intriguing, other studies conducted on animal models suggested that TRAIL is important in the prevention of autoimmune diseases and that a reduction of TRAIL activity could exacerbate autoimmune diseases and enhance proliferation of autoreactive lymphocytes.[3]

  In conclusion we failed to confirm a role of TRAIL as a disease specific molecule for SLE. A larger number of patients and a dosage of TRAIL receptors could be more precise and better reflect true TRAIL biological activity.

  References

  1. Matsuyama W, Yamamoto M, Higashimoto I, Oonakahara KI, Watanabe M, Machida K et al. TNF-related apoptosis-inducing ligand is involved in neutropenia of systemic lupus erythematosus. Blood 2004; 104:184-191.

  2. Rus V, Zernetkina V, Puliaev R, Cudrici C, Mathai S, Via CS. Increased expression and release of functional tumor necrosis factor- related apoptosis-inducing ligand (TRAIL) by T-cells from lupus patients with active disease. Clin Immunol 2005; 14 (Epub ahead of print).

  3. Song K, Chen Y, Goke R, Wilmen A, Seidel C, Goke A et al. Tumor necrosis factor related apoptosis-inducing ligand (TRAIL) is an inhibitor of autoimmune inflammation and cell cycle progression. J Exp Med 2000; 191: 1095-104.

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  Conflict of Interest:
  None declared.

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