Differences in tumor necrosis factor-α soluble receptor serum concentrations between patients with Henoch-Schonlein purpura and pediatric systemic lupus erythematosus: Pathogenetic implications

Marco Gattorno, Paolo Picco, Giancarlo Barbano, Franca Stalla, Maria Pia Sormani, Antonella Buoncompagni, Rosanna Gusmano, Carla Borrone, Vito Pistoia

Research output: Contribution to journalArticle

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Abstract

Objective. Animal models of immune complex mediated tissue injury have shown different patterns of proinflammatory cytokine production according to the subtype of immunoglobulin involved. The IgA immune complex model differs from the IgG model by the lack of involvement of tumor necrosis factor (TNF) in the pathogenesis of tissue damage. We investigated in age matched patients the possible difference in TNF involvement in a predominantly IgA mediated disease, Henoch-Schonlein purpura (HSP), in comparison with systemic lupus erythematosus (SLE), in which vascular injury is mostly associated with local deposition of IgG immune complexes. Methods. Serum concentrations of TNF-α and its soluble receptors (sTNF-R) p55 and p75 were studied in 20 patients with pediatric SLE at various degrees of disease activity, in 16 patients with highly active HSP, and in 15 healthy controls by enzyme amplified sensitivity immunoassay. SLE disease activity was evaluated using 2 scores, the European Consensus Group Study for SLE Disease Activity Criteria and the SLE Disease Activity Index. Results. Serum concentrations of TNF-α fell within the normal range in patients with both SLE and HSP irrespective of disease activity. Conversely, patients with SLE displayed increased serum levels of sTNF-R that correlated positively with the degree of disease activity (r = 0.60, p <0.001; r = 0.71, p <0.001, for p55 and p75, respectively). In contrast, no difference in the serum levels of sTNF-R was found between patients with highly active HSP and controls. Conclusion. Our study provides the first circumstantial evidence that pediatric SLE and HSP are characterized by differential involvement of TNF in the pathogenesis of tissue damage.

Original languageEnglish
Pages (from-to)361-365
Number of pages5
JournalJournal of Rheumatology
Volume25
Issue number2
Publication statusPublished - 1998

Fingerprint

Schoenlein-Henoch Purpura
Tumor Necrosis Factor Receptors
Systemic Lupus Erythematosus
Pediatrics
Serum
Tumor Necrosis Factor-alpha
Antigen-Antibody Complex
Immunoglobulin A
Immunoglobulin G
Vascular System Injuries
Immunoassay
Immunoglobulins
Reference Values
Animal Models
Cytokines
Wounds and Injuries
Enzymes

Keywords

  • Henoch-Schonlein purpura
  • Pediatric systemic lupus erythematosus
  • Tumor necrosis factor pathogenesis

ASJC Scopus subject areas

  • Rheumatology
  • Immunology

Cite this

Differences in tumor necrosis factor-α soluble receptor serum concentrations between patients with Henoch-Schonlein purpura and pediatric systemic lupus erythematosus : Pathogenetic implications. / Gattorno, Marco; Picco, Paolo; Barbano, Giancarlo; Stalla, Franca; Sormani, Maria Pia; Buoncompagni, Antonella; Gusmano, Rosanna; Borrone, Carla; Pistoia, Vito.

In: Journal of Rheumatology, Vol. 25, No. 2, 1998, p. 361-365.

Research output: Contribution to journalArticle

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abstract = "Objective. Animal models of immune complex mediated tissue injury have shown different patterns of proinflammatory cytokine production according to the subtype of immunoglobulin involved. The IgA immune complex model differs from the IgG model by the lack of involvement of tumor necrosis factor (TNF) in the pathogenesis of tissue damage. We investigated in age matched patients the possible difference in TNF involvement in a predominantly IgA mediated disease, Henoch-Schonlein purpura (HSP), in comparison with systemic lupus erythematosus (SLE), in which vascular injury is mostly associated with local deposition of IgG immune complexes. Methods. Serum concentrations of TNF-α and its soluble receptors (sTNF-R) p55 and p75 were studied in 20 patients with pediatric SLE at various degrees of disease activity, in 16 patients with highly active HSP, and in 15 healthy controls by enzyme amplified sensitivity immunoassay. SLE disease activity was evaluated using 2 scores, the European Consensus Group Study for SLE Disease Activity Criteria and the SLE Disease Activity Index. Results. Serum concentrations of TNF-α fell within the normal range in patients with both SLE and HSP irrespective of disease activity. Conversely, patients with SLE displayed increased serum levels of sTNF-R that correlated positively with the degree of disease activity (r = 0.60, p <0.001; r = 0.71, p <0.001, for p55 and p75, respectively). In contrast, no difference in the serum levels of sTNF-R was found between patients with highly active HSP and controls. Conclusion. Our study provides the first circumstantial evidence that pediatric SLE and HSP are characterized by differential involvement of TNF in the pathogenesis of tissue damage.",
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N2 - Objective. Animal models of immune complex mediated tissue injury have shown different patterns of proinflammatory cytokine production according to the subtype of immunoglobulin involved. The IgA immune complex model differs from the IgG model by the lack of involvement of tumor necrosis factor (TNF) in the pathogenesis of tissue damage. We investigated in age matched patients the possible difference in TNF involvement in a predominantly IgA mediated disease, Henoch-Schonlein purpura (HSP), in comparison with systemic lupus erythematosus (SLE), in which vascular injury is mostly associated with local deposition of IgG immune complexes. Methods. Serum concentrations of TNF-α and its soluble receptors (sTNF-R) p55 and p75 were studied in 20 patients with pediatric SLE at various degrees of disease activity, in 16 patients with highly active HSP, and in 15 healthy controls by enzyme amplified sensitivity immunoassay. SLE disease activity was evaluated using 2 scores, the European Consensus Group Study for SLE Disease Activity Criteria and the SLE Disease Activity Index. Results. Serum concentrations of TNF-α fell within the normal range in patients with both SLE and HSP irrespective of disease activity. Conversely, patients with SLE displayed increased serum levels of sTNF-R that correlated positively with the degree of disease activity (r = 0.60, p <0.001; r = 0.71, p <0.001, for p55 and p75, respectively). In contrast, no difference in the serum levels of sTNF-R was found between patients with highly active HSP and controls. Conclusion. Our study provides the first circumstantial evidence that pediatric SLE and HSP are characterized by differential involvement of TNF in the pathogenesis of tissue damage.

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