It is believed that IL-15 might contribute to autoimmune diseases by inducing the expression of TNF-α, by inhibiting self-tolerance mediated by IL-2-induced AICD, and by facilitating the maintenance of CD8 memory T cell survival, including that of self-reactive memory cells. For example, dysregulated IL-15 expression has been reported in patients with a range of autoimmune diseases such as multiple sclerosis, inflammatory bowel disease and psoriasis. In this context, cytokine-directed blockade of TNF with specific monoclonal antibodies or soluble TNF receptors has been an important target for many of the diseases mention previously. Yet TNF-directed therapies do not provide effective therapy for all these patients, and new theurapeutic targets are needed. Furthermore, although TNF-directed therapy has an anti-inflammatory effect, it does not have an effect on self-reactrive memory T cells that might play a role in the pathogenesis and maintenance of autoimmune diseases. Thus, it is hoped that by targeting IL-15 it might be possible to both achieve the anti-inflammatory effects and reduce the number of CD8 self-reactive memort T cells.
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