RT Journal Article
SR Electronic
T1 Cutting Edge: Anti-Tumor Necrosis Factor Therapy in Rheumatoid Arthritis Inhibits Memory B Lymphocytes via Effects on Lymphoid Germinal Centers and Follicular Dendritic Cell Networks
JF The Journal of Immunology
JO J. Immunol.
FD American Association of Immunologists
SP 688
OP 692
DO 10.4049/jimmunol.180.2.688
VO 180
IS 2
A1 Anolik, Jennifer H.
A1 Ravikumar, Rajan
A1 Barnard, Jennifer
A1 Owen, Teresa
A1 Almudevar, Anthony
A1 Milner, Eric C. B.
A1 Miller, Chase H.
A1 Dutcher, Paul O.
A1 Hadley, James A.
A1 Sanz, Iñaki
YR 2008
UL http://www.jimmunol.org/content/180/2/688.abstract
AB Rheumatoid arthritis (RA) is mediated by a proinflammatory cytokine network with TNF at its apex. Accordingly, drugs that block TNF have demonstrated significant efficacy in the treatment of RA. A great deal of experimental evidence also strongly implicates B cells in the pathogenesis of RA. Yet, it remains unclear whether these two important players and the therapies that target them are mechanistically linked. In this study we demonstrate that RA patients on anti-TNF (etanercept) display a paucity of follicular dendritic cell networks and germinal center (GC) structures accompanied by a reduction in CD38+ GC B cells and peripheral blood memory B cell lymphopenia compared with healthy controls and RA patients on methotrexate. This study provides initial evidence in humans to support the notion that anti-TNF treatment disrupts GC reactions at least in part via effects on follicular dendritic cells.