mbt scarpe prezzi Immune pathogenesis of psoriasis

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Immune pathogenesis of psoriasis and immunotherapy

Inhibition is likely to be generated by lymphocyte cytokines play a role in reducing CsA indirectly bind to intracellular receptor proteins on the ring, forming a ring of CsA protein complex. This compound inhibiting calcineurin, then inhibition of NFAT in the cytoplasm to the nucleus subunit translocation through the nuclear membrane. Because NFAT transcription of IL-2 is important, therefore, CsA application will result in the disappearance of IL-2,[link widoczny dla zalogowanych], thereby preventing the activation of T cell proliferation, the purpose to control the symptoms of psoriasis. FKS06 as a kind of macrolides antibiotics. CsA different in structure, but with almost the same cellular role. With immune globulin FKBP (FK binding protein) to form a FKBP FK506 complexes that complex cells by blocking the calcium-dependent information transfer,[link widoczny dla zalogowanych], thus inhibiting antigen-induced T-cell activation. FK506 on keratinocytes by 40 students have no direct role. Ray afraid of mold claims (rapamycin) is another antibiotic macrolides tired. Also binds to FKBP,[link widoczny dla zalogowanych], but does not inhibit calcineurin and cytokine synthesis,[link widoczny dla zalogowanych], and inhibition of cytokine-mediated signal transduction, and even IL-2 receptor signal transduction inhibition discretion (ie, inhibition of S-6 kinase ) high specific immune inhibitors: the process of antigen presenting T cells to determine the further understanding of the high specificity of the role of immunosuppressive Jing target site possible. Reports indicate that the system with anti-CD4 monoclonal antibodies can eliminate or significantly improve psoriasis symptoms. But its shortcomings, including the possible immunogenicity of the antibody; lack of selectivity resulting CD ~ + T cells in the universality of failure,[link widoczny dla zalogowanych], and disease recurrence after stopping treatment. Advantage of T cells in psoriatic plaque clone V-port extended to the high specific immunotherapy prompted another target. Eye and mouth antigen induced antigen-specific immune tolerance is another way. Biological response modifying factor: application of cytokines such as TNF-n can eliminate the symptoms of psoriasis. This result seems paradoxical, because TNF-a in psoriasis is an important evolution of the primary media. However, there may be super-physiological levels of TNF-would cut its receptor, resulting in a suppression role. Presumably, psoriasis as a TH1 cell-mediated diseases through the application of TH 2 cells around a child, that IL-lO, or IL-4 to the improvement of clinical symptoms and may become a treatment for psoriasis countermeasures. In addition, anti-cytokine therapy for psoriasis Methods Summary existence of another potential sign of support for many of T lymphocytes and other immune cells in psoriatic disease mechanisms on the importance of the boat. But it is not clear that the keratinocyte proliferation in the process of its own whether to play a starting role. Basic science research to enable people to better understanding of a variety of cellular and molecular changes. So that the immune pharmacologist can stare them in different ways changes the immune needle therapy. To believe. Theory of the immune pathogenesis of psoriasis with the rapid development of the most selective immune therapy will soon become a reality.
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