Increase of B Cell-activating Factor of the TNF Family (BAFF) After Rituximab Treatment: Insights into a New Regulating System of BAFF Production

Overview

Journal Ann Rheum Dis

Specialty Rheumatology

Date 2006 Oct 17

PMID 17040963

Citations 78

Authors

Frederic Lavie

Corinne Miceli-Richard

Marc Ittah

Jeremie Sellam

Jacques-Eric Gottenberg

Xavier Mariette

Affiliations

Soon will be listed here.

Abstract

Background: The cytokine B cell-activating factor of the TNF family (BAFF) is involved in the pathogenesis of autoimmune diseases.

Objective: To access changes in serum protein and mRNA levels of BAFF after rituximab treatment.

Methods: Serum and peripheral blood mononuclear cells (PBMCs) were isolated from five patients (two with lupus, two with Sjögren's syndrome, one with rheumatoid arthritis) before and 12 weeks (range 7-17) after a first course of rituximab infusion. Monocytes and B cells were selected from healthy controls and cocultured for 72 h. BAFF protein and mRNA levels were assessed by ELISA and real-time PCR, respectively.

Results: After rituximab treatment, median serum BAFF protein level and BAFF to actin mRNA ratio in PBMCs significantly increased. In monocytes cocultured with autologous B cells, BAFF protein level decreased, whereas the mRNA level was stable. In one closely monitored patient, the mRNA ratio of BAFF to actin in PBMCs increased later than the BAFF serum level.

Conclusions: Two distinct mechanisms are probably involved in the increase in BAFF level after B cell depletion: (1) the decrease in its receptors leading to a release of BAFF; (2) a delayed regulation of BAFF mRNA transcription. This could favour the re-emergence of autoreactive B cells.

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