Daclizumab is a humanized mAb against CD25, the alpha chain of the interleukin-2 receptor. CD25 is expressed on a subset of T cells. Anti-CD25 treatment aims to limit T-cell proliferation by blocking IL-2 signaling via its high affinity receptor. Two open-label phase 2 studies showed that daclizumab is well tolerated and leads to a significant reduction of MRI activity and significant improvement of several clinical outcome mea sures, also in patients with only incomplete response to interferon therapy (Bielekova et al. 2004). Surprisingly, the treatment led to only mild functional blockade of CD4 positive T cells. Instead administration of daclizumab resulted in a significant expansion of CD56 bright natural killer (NK) cells (Bielekova et al. 2006). These recent data provide evidence to support the existence of an immunoregulatory pathway wherein activated NK cells inhibit T-cell survival. Thus this approach may have potential implications for future MS therapy.
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