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Blood, 1 June 2008, Vol. 111, No. 11, pp. 5334-5341.
Prepublished online as a Blood First Edition Paper on February 21, 2008; DOI 10.1182/blood-2007-11-122713.
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Submitted November 7, 2007
Accepted February 17, 2008
Restoration of peripheral immune homeostasis after Rituximab in mixed cryoglobulinemia vasculitis
David Saadoun, Michelle Rosenzwajg, Dan Landau, Jean Charles Piette, David Klatzmann, and Patrice Cacoub*
Laboratoire de Biologie et Therapeutique des Pathologies Immunitaires, CNRS/UPMC UMR 7087, Universite Pierre et Marie Curie, Paris, France
Service de Medecine Interne, Hopital Pitie-Salpetriere, Universite Pierre et Marie Curie, Paris, France
* Corresponding author; email: patrice.cacoub{at}psl.aphp.fr.
Rituximab, an anti-CD20 monoclonal antibody has been used to treat autoimmune disorders such as mixed cryoglobulinemia (MC). However, its mechanisms of action as well as the effects on cellular immunity remain poorly defined. We investigated the changes of peripheral blood B and T cell subsets, the clonal VH1-69 cells as well as the cytokine profile following rituximab therapy. The study involved 21 patients with hepatitis C-related MC who received rituximab, of whom 14 achieved a complete response. Compared with healthy and HCV controls, pretreatment abnormalities in MC patients included a decreased percentage of naive B cells (p<0.05) and CD4+CD25+FoxP3+ regulatory T cells (p=0.02) with an increase in memory B cells (p=0.03) and plasmablast (p<0.05). These abnormalities were reverted at 12 months after rituximab. Clonal VH1-69+ B cells dramatically decreased following treatment (32 ± 6% versus 8 ± 2%, p=0.01). Complete responders of rituximab exhibited an expansion of regulatory T cells (p<0.01) accompanies with a decrease in CD8+ T cell activation (p<0.01) and decreased production of IL-12 (p=0.02) and IFN- (p=0.01). Our findings indicate that in patients with MC response to B cell depletion induced by rituximab effectively normalizes many of the disturbances in peripheral B and T lymphocyte homeostasis.
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