A molecule solves @entity1569 ? Systemic therapies for @entity1569 inducing XXXX and Th2 responses.

@entity404 @entity1569 @entity1198 @entity379 @entity6897 @entity3646 @entity792
Psoriasis is an @entity792 affecting 2-4% of the Caucasian population. Inflammatory processes induce the migration of @entity379 producing @entity1198 lymphocytes into the skin. These play a key role in the pathogenesis of @entity1569 . These @entity1198 lymphocytes are responsible for the pathological reactions in psoriatic skin leading to keratinocyte hyperproliferation, small vessel proliferation and neutrophilic infiltration. Antigen-presenting cells activate dermal @entity404 + T lymphocytes, and various signals can support the polarization of @entity1198 responses. The main signal for @entity1198 development is interleukin (IL) 12. After binding to their receptors both IL-12 and @entity379 promote intracellular @entity379 production by activating signal transducer and activator of transcription (STAT) 4 or 1. @entity6897 activation by @entity379 is followed by T-bet activation, a master transcription factor for @entity1198 lymphocytes. In experimental models of @entity1198 -mediated @entity792 immune deviation of polarized autoreactive @entity1198 into anti-inflammatory Th2 responses generally improves the disease. Therefore new therapeutic approaches based on immunomodulating molecules have been developed for @entity1569 , a prototypical @entity1198 -mediated @entity792 . Recently @entity3646 , the most effective Th2-inducing cytokine, has been shown to be safe and efficient for treating @entity1569 . Improvement was associated with the induction of a Th2 phenotype of skin infiltrating lymphocytes. This review summarizes the @entity3646 inducing potential of various conventional and newer systemic therapies for @entity1569 . Many of these were thought to be primarily immunosuppressive. A review of the literature reveals that most of them can induce @entity3646 and Th2, and that Th2 induction may be an underestimated mode of action in the therapy of @entity1198 -mediated @entity792 . Further studies are needed to determine the central role of @entity3646 in the control of @entity1198 -induced @entity792 , namely @entity1569 .
