Anti-tumor necrosis factor-α response in rheumatoid arthritis is associated with an increase in serum soluble CD30

Roberto Gerli, Claudio Lunardi, Elena Bartoloni Bocci, Francesca Bobbio-Pallavicini, Giuseppe Schillaci, Roberto Caporali, Onelia Bistoni, Matteo Pirro, Costantino Pitzalis, Carlomaurizio Montecucco

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

Objective. Patients with rheumatoid arthritis (RA) display high serum concentrations of soluble CD30 (sCD30), which correlate with counter-regulatory activity of CD30+ T cells in the inflamed joint. To verify the contribution of this T cell subset to disease remission, sCD30 levels were analyzed longitudinally in patients with active RA following infliximab therapy. Methods. Infliximab plus methotrexate were started in 39 patients with active RA, while 20 patients with inactive disease, controlled by stable doses of methotrexate, acted as controls. Serial evaluations of sCD30 concentrations and disease activity indexes were performed throughout 38 weeks. Results. sCD30 levels were higher in patients than in healthy controls. Rapid infliximab-induced decrease in disease activity was associated with an overall increase of sCD30 levels. In contrast, levels remained stable in controls. An inverse correlation between sCD30 levels and Disease Activity Score 28 was observed from the 22nd week of infliximab treatment. Analysis of sCD30 levels according to American College of Rheumatology response showed, after an initial general enhancement of sCD30 concentrations, a persistent increase of sCD30 in responders, but not in nonresponders. Conclusion. sCD30 serum levels are enhanced by tumor necrosis factor-α (TNF-α) blockade in patients with active RA and inversely correlated with disease activity, but only after some weeks of treatment. Of interest, a sustained increase of sCD30 is present only in subjects with evidence of persistent clinical response to anti-TNF-α. As sCD30 serum levels mirror antiinflammatory activity of joint T cells, the present data may suggest a role of synovial counter-regulatory CD30+ T cells in the induction of infliximab-mediated remission in RA.

Original languageEnglish
Pages (from-to)14-19
Number of pages6
JournalJournal of Rheumatology
Volume35
Issue number1
Publication statusPublished - Jan 2008

Fingerprint

Rheumatoid Arthritis
Tumor Necrosis Factor-alpha
Serum
Methotrexate
Joints
T-Lymphocytes
T-Lymphocyte Subsets
Regulatory T-Lymphocytes
Anti-Inflammatory Agents
Therapeutics
Infliximab

Keywords

  • Anti-tumor necrosis factor-α
  • CD30
  • Infliximab
  • Rheumatoid arthritis
  • T cells

ASJC Scopus subject areas

  • Rheumatology
  • Immunology

Cite this

Anti-tumor necrosis factor-α response in rheumatoid arthritis is associated with an increase in serum soluble CD30. / Gerli, Roberto; Lunardi, Claudio; Bocci, Elena Bartoloni; Bobbio-Pallavicini, Francesca; Schillaci, Giuseppe; Caporali, Roberto; Bistoni, Onelia; Pirro, Matteo; Pitzalis, Costantino; Montecucco, Carlomaurizio.

In: Journal of Rheumatology, Vol. 35, No. 1, 01.2008, p. 14-19.

Research output: Contribution to journalArticle

Gerli, Roberto ; Lunardi, Claudio ; Bocci, Elena Bartoloni ; Bobbio-Pallavicini, Francesca ; Schillaci, Giuseppe ; Caporali, Roberto ; Bistoni, Onelia ; Pirro, Matteo ; Pitzalis, Costantino ; Montecucco, Carlomaurizio. / Anti-tumor necrosis factor-α response in rheumatoid arthritis is associated with an increase in serum soluble CD30. In: Journal of Rheumatology. 2008 ; Vol. 35, No. 1. pp. 14-19.
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title = "Anti-tumor necrosis factor-α response in rheumatoid arthritis is associated with an increase in serum soluble CD30",
abstract = "Objective. Patients with rheumatoid arthritis (RA) display high serum concentrations of soluble CD30 (sCD30), which correlate with counter-regulatory activity of CD30+ T cells in the inflamed joint. To verify the contribution of this T cell subset to disease remission, sCD30 levels were analyzed longitudinally in patients with active RA following infliximab therapy. Methods. Infliximab plus methotrexate were started in 39 patients with active RA, while 20 patients with inactive disease, controlled by stable doses of methotrexate, acted as controls. Serial evaluations of sCD30 concentrations and disease activity indexes were performed throughout 38 weeks. Results. sCD30 levels were higher in patients than in healthy controls. Rapid infliximab-induced decrease in disease activity was associated with an overall increase of sCD30 levels. In contrast, levels remained stable in controls. An inverse correlation between sCD30 levels and Disease Activity Score 28 was observed from the 22nd week of infliximab treatment. Analysis of sCD30 levels according to American College of Rheumatology response showed, after an initial general enhancement of sCD30 concentrations, a persistent increase of sCD30 in responders, but not in nonresponders. Conclusion. sCD30 serum levels are enhanced by tumor necrosis factor-α (TNF-α) blockade in patients with active RA and inversely correlated with disease activity, but only after some weeks of treatment. Of interest, a sustained increase of sCD30 is present only in subjects with evidence of persistent clinical response to anti-TNF-α. As sCD30 serum levels mirror antiinflammatory activity of joint T cells, the present data may suggest a role of synovial counter-regulatory CD30+ T cells in the induction of infliximab-mediated remission in RA.",
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AU - Gerli, Roberto

AU - Lunardi, Claudio

AU - Bocci, Elena Bartoloni

AU - Bobbio-Pallavicini, Francesca

AU - Schillaci, Giuseppe

AU - Caporali, Roberto

AU - Bistoni, Onelia

AU - Pirro, Matteo

AU - Pitzalis, Costantino

AU - Montecucco, Carlomaurizio

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N2 - Objective. Patients with rheumatoid arthritis (RA) display high serum concentrations of soluble CD30 (sCD30), which correlate with counter-regulatory activity of CD30+ T cells in the inflamed joint. To verify the contribution of this T cell subset to disease remission, sCD30 levels were analyzed longitudinally in patients with active RA following infliximab therapy. Methods. Infliximab plus methotrexate were started in 39 patients with active RA, while 20 patients with inactive disease, controlled by stable doses of methotrexate, acted as controls. Serial evaluations of sCD30 concentrations and disease activity indexes were performed throughout 38 weeks. Results. sCD30 levels were higher in patients than in healthy controls. Rapid infliximab-induced decrease in disease activity was associated with an overall increase of sCD30 levels. In contrast, levels remained stable in controls. An inverse correlation between sCD30 levels and Disease Activity Score 28 was observed from the 22nd week of infliximab treatment. Analysis of sCD30 levels according to American College of Rheumatology response showed, after an initial general enhancement of sCD30 concentrations, a persistent increase of sCD30 in responders, but not in nonresponders. Conclusion. sCD30 serum levels are enhanced by tumor necrosis factor-α (TNF-α) blockade in patients with active RA and inversely correlated with disease activity, but only after some weeks of treatment. Of interest, a sustained increase of sCD30 is present only in subjects with evidence of persistent clinical response to anti-TNF-α. As sCD30 serum levels mirror antiinflammatory activity of joint T cells, the present data may suggest a role of synovial counter-regulatory CD30+ T cells in the induction of infliximab-mediated remission in RA.

AB - Objective. Patients with rheumatoid arthritis (RA) display high serum concentrations of soluble CD30 (sCD30), which correlate with counter-regulatory activity of CD30+ T cells in the inflamed joint. To verify the contribution of this T cell subset to disease remission, sCD30 levels were analyzed longitudinally in patients with active RA following infliximab therapy. Methods. Infliximab plus methotrexate were started in 39 patients with active RA, while 20 patients with inactive disease, controlled by stable doses of methotrexate, acted as controls. Serial evaluations of sCD30 concentrations and disease activity indexes were performed throughout 38 weeks. Results. sCD30 levels were higher in patients than in healthy controls. Rapid infliximab-induced decrease in disease activity was associated with an overall increase of sCD30 levels. In contrast, levels remained stable in controls. An inverse correlation between sCD30 levels and Disease Activity Score 28 was observed from the 22nd week of infliximab treatment. Analysis of sCD30 levels according to American College of Rheumatology response showed, after an initial general enhancement of sCD30 concentrations, a persistent increase of sCD30 in responders, but not in nonresponders. Conclusion. sCD30 serum levels are enhanced by tumor necrosis factor-α (TNF-α) blockade in patients with active RA and inversely correlated with disease activity, but only after some weeks of treatment. Of interest, a sustained increase of sCD30 is present only in subjects with evidence of persistent clinical response to anti-TNF-α. As sCD30 serum levels mirror antiinflammatory activity of joint T cells, the present data may suggest a role of synovial counter-regulatory CD30+ T cells in the induction of infliximab-mediated remission in RA.

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