The pathogenesis of psoriasis can be explained by dysregulation of immunological cell function as well as keratinocyte proliferation/differentiation. Recently, the immunological pathomechanism has been clarified substantially. Whereas T-helper (Th)1 overactivation was thought to induce occurrence of psoriasis, it has been demonstrated that Th17 cells play a key role. Th17 development is maintained by interleukin (IL)-23 mainly produced by dendritic cells. Th17 cells produce various cytokines, including IL-17A, IL-17F and IL-22. IL-17A and IL-22 induce not only keratinocyte proliferation, but also tumor necrosis factor (TNF)-a, chemokine (C-X-C motif) ligand (CXCL)1 and CXCL8 production. TNF-a accelerates the infiltration of inflammatory cells, including lymphocytes, monocytes and neutrophils, from the peripheral blood into skin with dendritic cell activation. In addition, antimicrobial peptides are overexpressed in psoriatic skin lesions, and the antimicrobial peptide, LL-37, activates dendritic cells, which leads to the development of inflammation. Furthermore, activation of nuclear factor-jB signal induces the expression of keratins 6 and 16 in keratinocytes, which are associated with acanthosis and reduced turnover time in the epidermis. The progression of the pathomechanism contributes to the development of new therapies for psoriasis.
We present a theoretical understanding of the superconducting phase diagram of the electron-doped iron pnictides. We show that, besides the Fermi surface nesting, a peculiar motion of electrons, where the next nearest neighbor (diagonal) hoppings between iron sites dominate over the nearest neighbor ones, plays an important role in the enhancement of the spin fluctuation and thus superconductivity. In the highest T(c) materials, the crossover between the Fermi surface nesting and this "prioritized diagonal motion" regime occurs smoothly with doping, while in relatively low T(c) materials, the two regimes are separated and therefore results in a double dome T(c) phase diagram.
A molecular theory is presented in this paper which gives a method of analysis for the mechanical properties of filler-reinforced elastomers, based upon the concept of the internal deformation and the statistical theory of rubberlike elasticity. By using a suitable model and a few new concepts a proper analysis for such a heterogeneous system is obtained. From the theory the internal mechanism of filler reinforcement is understood. It is made clear that reinforcement consists of three effects: the volume effect, the surface effect, and the cavitation effect. From the theory, formulae for the tension, swelling tension, Young's moduli, local stress distribution, strain birefreingence, condition for swelling equilibrium, and so on are derived. It has long been recognized that rubbery substances and plastic materials are reinforced by incorporation of suitable powdery substances (reinforcing fillers) which improve their mechanical properties such as elastic modulus, hardness, stiffness, resilience, solvent resistance, plastic viscosity, tensile strength, tear resistance, etc. Although numerous attempts have been made to clarify and systematize the internal mechanism of filler reinforcement, there is at present no distinct picture of the mechanism, much less a satisfactory theoretical treatment of the phenomena.
Psoriasis is a chronic inflammatory skin condition caused by a combination of hereditary and environmental factors. Its development is closely related to the adaptive immune response. T helper 17 cells are major IL-17-producing cells, a function that plays an important role in the pathogenesis of psoriasis. However, recent findings have demonstrated that innate immune cells also contribute to the development of psoriasis. Innate lymphoid cells, γδ T cells, natural killer T cells, and natural killer cells are activated in psoriasis, contributing to disease pathology through IL-17-dependent and -independent mechanisms. The present review provides an overview of recent findings, demonstrating a role for innate immunity in psoriasis.
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