Research ArticleMultiple Sclerosis

Inhibition of LTi Cell Development by CD25 Blockade Is Associated with Decreased Intrathecal Inflammation in Multiple Sclerosis

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Science Translational Medicine  01 Aug 2012:
Vol. 4, Issue 145, pp. 145ra106
DOI: 10.1126/scitranslmed.3004140

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The Innate Talent of Daclizumab

Watching an Olympic medalist excel at his or her chosen event is a thing of beauty. Yet when it comes to analyzing these superior performances, opinions differ on the relative contributions of innate talent versus targeted training. In the debilitating autoimmune disease multiple sclerosis (MS), T lymphocytes—adaptive immune cells—have long been thought to be one of the main culprits. However, a new study by Perry et al. suggests that the humanized monoclonal antibody daclizumab decreases MS-associated inflammation partly through its inhibitory effects on innate rather than adaptive lymphoid cells. Daclizumab has a direct but limited ability to block the function of CD25, a receptor that is up-regulated on activated T cells, including those involved in autoimmune disease. In the new work, the authors turned their attention to innate lymphoid cells (ILCs), components of the other branch of the immune system, and found higher numbers of circulating ILCs in untreated MS patients compared with daclizumab-treated ones. Indeed, daclizumab therapy modified this cell population, skewing it toward a more immunoregulatory cell type. Thus, daclizumab may indirectly modulate activated T cells by altering the regulatory effects of ILCs on the adaptive immune system. Therapies that specifically target ILCs represent a new avenue of therapeutic research for MS and perhaps other autoimmune diseases as well. If this research crosses the translational finish line, MS patients will take home the gold.