| Summary: | <p>Abstract</p> <p>Background</p> <p>Alefacept (anti-CD2) biological therapy selectively targets effector memory T cells (Tem) in psoriasis vulgaris, a model Type 1 autoimmune disease.</p> <p>Methods</p> <p>Circulating leukocytes were phenotyped in patients receiving alefacept for moderate to severe psoriasis.</p> <p>Results</p> <p>In all patients, this treatment caused a preferential decrease in effector memory T cells (CCR7<sup>- </sup>CD45RA<sup>-</sup>) (mean 63% reduction) for both CD4<sup>+ </sup>and CD8<sup>+ </sup>Tem, while central memory T cells (Tcm) (CCR7<sup>+</sup>CD45RA<sup>-</sup>) were less affected, and naïve T cells (CCR7<sup>+</sup>CD45RA<sup>+</sup>) were relatively spared. Circulating CD8<sup>+ </sup>effector T cells and Type 1 T cells (IFN-γ-producing) were also significantly reduced.</p> <p>Conclusion</p> <p>Alefacept causes a selective reduction in circulating effector memory T cells (Tem) and relative preservation of central memory T cells (Tcm) in psoriasis.</p>
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