Identification of chemokines and cytokines offers new hope for inflammatory myopathy patients

The inflammatory myopathies comprise three different entities: polymyositis, inclusion body myositis and dermatomyositis. People in all age groups can be affected by major muscle weakness and pain, and show evidence of muscle fiber breakdown in the serum. Autoimmune pathogenetic mechanisms have been identified in each inflammatory myopathy, but the antigen(s) recognized by the autoreactive inflammatory cells and the factors eliciting the aberrant immune responses remain unknown. Currently, patients are treated with corticosteroids with variable success rates and at a high cost of side-effects.

The ongoing research is aimed at identifying the factors that guide the trafficking of inflammatory cells from the blood to the inflamed muscle tissue. A new study reports the differential expression of chemokines and their receptors in each inflammatory myopathy. Chemokines represent a family of small-molecular weight cytokines that have an important role in the migration of distinct leukocyte subsets to the sites of inflammation. The chemokines monocyte chemoattractant protein-1 (MCP-1) and stromal derived factor (SDF-1a and SDF-1b) and their receptors are strongly expressed whereas a number of others are undetectable.

Blocking the autoimmune cascade by targeting chemokines or chemokine receptors has given excellent results in animal models of other immune diseases. The present work identifies the candidates for selective immune intervention in patients suffering autoimmune inflammatory myopathies and may well lead to more selective treatment modalities with less side-effects than the currently available drugs.

Previous research by this group had focused on other factors that control recruitment and activation of immune cells, such as cell adhesion molecules and cytokines. Based in part on data that described the role of the cytokine tumor necrosis factor-a (TNF-a) and its receptors in inflammatory myopathy muscle biopsies, preliminary clinical studies with TNF-blocking monoclonal antibodies are now being initiated in several hospitals. “It is very encouraging to see data obtained from clinically oriented research move from the laboratory bench to the clinical treatment phase in just a few years time”, said Professor Jan De Bleecker who is the first author of these papers.

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Jan DE BLEECKER alfa

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