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.

Agenesis of lung is a rare congenital disorder. We are reporting varied degree of pulmonary agenesis in two adult patients.

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Rheumatoid arthritis (RA) is a systemic autoimmune disease that is associated with immunologic alterations in T cells and B cells. Moreover, many of the agents used in RA patients are potentially immunosuppressive. Thus, the underlying disease and treatment may both increase the susceptibility to infections and decrease vaccine responses. With the growing use of aggressive therapies for RA, including anti-tumor necrosis factor agents and newer biologic therapies such as rituximab and abatacept, an increasing concern will be that patients may not respond to conventional vaccination. Further prospective studies on response to vaccination are needed to answer this important public health question. Nevertheless, it is already clear that vaccination does induce response in many patients. Unfortunately, vaccination is underutilized in RA patients and needs to be aggressively promoted.