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

The article offers information on a randomized clinical trial conducted to observe the activity of GS-5806, which is an inhibitor of respiratory syncytial virus (RSV) that leads to infant hospitalizations, morbidity and mortality. It states that the participants were divided into two groups, one received GS-5806 and other received placebo. It concludes that the treatment of infants with GS-5806 reduced the viral load of RSV.

The article discusses a study which evaluated the safety and efficacy of eight years etanercept treatment in patients diagnosed with polyarticular-course juvenile rheumatoid arthritis (JRA). The study included JRA patients who were previous participants of a randomized controlled trial (RCT) of etanercept. No cases of opportunistic infections, lupus, lymphomas or deaths were reported among the study population. The study concluded that the acceptable safety profile of etanercept is maintained for up to eight years.

We find that CD11c+ cells with many markers of dendritic cells (DCs) are a major cell type in the skin lesions of psoriasis. These CD11c+ cells, which are evident in both epidermis and dermis, are the sites for the expression of two mediators of inflammation, inducible nitric oxide synthase (iNOS) and TNF-α in diseased skin. These cells express HLA-DR, CD40, and CD86, lack the Langerin and CD14 markers of Langerhans cells and monocytes, respectively, and to a significant extent express the DC maturation markers DC- LAMP and CD83. Treatment of psoriasis with efalizumab (anti- CD11a, Raptiva) strongly reduces infiltration by these DCs in patients responding to this agent. Disease activity after therapy was more related to DC infiltrates and iNOS mRNA levels than T cell infiltrates, and CD11c+ cells responded more quickly to therapy than epidermal keratinocytes. Our results suggest that a type of DC, which resembles murine "Tip-DC5" that can accumulate during infection, has proinflammatory effects in psoriasis through nitric oxide and TNF-α production, and can be an important target for suppressive therapies. [ABSTRACT FROM AUTHOR]