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Why are female athletes more susceptible to knee ligament injuries than male athletes performing the same activities? Several theories have been put forward to explain this phenomenon.
A rare but often fatal viral disease has been reported in a number of patients treated with rituximab, but how the risk of this complication should affect prescription practices demands consideration of several important factors.
Biologic therapies that target interleukin (IL)-1 are known to dramatically improve symptoms of a group of rare, heritable chronic inflammatory diseases. The results of a phase III trial confirm the place of canakinumab in the treatment arsenal for these disorders.
The therapeutic options for patients with rheumatoid arthritis (RA) have changed dramatically over the past two decades, as discussed in this Review. The current landscape of RA therapy in terms of available therapeutics is described, and accepted principles of RA management and some important controversies in this field are outlined.
Current therapies for RA focus on inhibition of synovitis, but do not adequately repair the bone damage that results from the imbalance of the osteoblast–osteoclast axis. Targeting key molecules involved in osteoclastogenesis and osteoblastogenesis might reduce bone destruction and enhance repair of erosions in this disease.
Interleukin-17 has been implicated in the pathogenesis of inflammatory arthritis. Evidence from animal models and preliminary results from trials in human disease highlight the emergence of this proinflammatory cytokine as a target for RA therapy.
G-CSF and GM-CSF are well-known regulators of hematopoiesis, but these cytokines also have proinflammatory activity and are expressed in the joints of patients with rheumatoid arthritis. Antagonism of G-CSF or GM-CSF might represent a novel, safe and effective way of treating this disease.
Regulatory T cells are critically involved in immune homeostasis. Several established and experimental treatments for RA might work via effects on regulatory T cells. This Review discusses the potential benefits and pitfalls of targeting these cells to control autoimmunity.
Dendritic cells have a crucial role in inducing immunity and mediating immune tolerance. Current biologic therapies for RA target some of the cytokine products of dendritic cells, whereas emerging therapies are aimed at exploiting their tolerogenic capacity.
Monoclonal antibodies directed against CD20 have emerged as an effective therapy for RA. Using this approach to target CD19 could provide a greater breadth of B-cell depletion with additional therapeutic benefits.
Tumor necrosis factor (TNF) is expressed at high levels in synovial tissue from patients with RA. Through preclinical studies, animal model studies and human trials, this cytokine was the first to be fully validated as a therapeutic target for RA. Several approaches to blocking TNF have been developed, demonstrating considerable benefit in most of the patients treated.
Premature aging of the immune system, driven by defective DNA maintenance and repair, could be responsible for the pathogenesis of RA. The authors discuss the phenomenon of premature immunosenescence in RA, and suggest that 'resetting' the immune system could be a novel therapeutic concept.
This Focus issue on the future of therapy for rheumatoid arthritis (RA) contains a specially commissioned lead Review on the current state-of-the-art therapeutic approaches for RA and a series of shorter Review articles that introduce some new molecules and cells identified by the leaders in this field as the next promising targets for this disease.
