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KEYWORDS: IL-23 axis innate immunity psoriasis skin barrier Th17

KEYWORDS: IL-23 axis  innate immunity  psoriasis  skin barrier  Th17 1

Psoriasis is a common, immunologically mediated, inflammatory and hyperproliferative disease of the skin and joints, with a multifactorial genetic basis. Keywords:. The discovery that inducible T-cell costimulator and IL-23 selectively regulate IL-17A-producing CD4+ T cells suggests that these cells are a separate helper cell subset. In addition to Th17 cells, there are several types of innate immune cells that also produce IL-17A and IL-17F, among which T cells are the best understood. T cells are the exclusive source of IL-17A and IL-17F in skin lesions. Keratinocytes can be viewed as an integral part of the skin-resident immune system, because they may act as APCs, produce innate immune mediators, and contribute to the skin homing and local activation of immune cells.

KEYWORDS: IL-23 axis  innate immunity  psoriasis  skin barrier  Th17 2Keywords: Psoriasis, eczema, gene expression, NOS2 gene, CCL27 gene, disease classifier. Concerning innate immune response, eczema seems to be associated with NOD1, NOD2, TLR2, CD14, and DEFB1 genes, and psoriasis with TNFAIP3 and TNIP1, which participate in tumor necrosis factor (TNF) signaling and regulation of the transcription nuclear factor kB (NF-kB). Abnormal skin barrier in the etiopathogenesis of atopic dermatitis. Expanding the psoriasis disease profile: interrogation of the skin and serum of patients with moderate-to-severe psoriasis. Human keratinocytes’ response to injury upregulates CCL20 and other genes linking innate and adaptive immunity. 46Roberson, E.D. and Bowcock, A.M. Psoriasis genetics: breaking the barrier. The IL23R R381Q gene variant protects against immune-mediated diseases by impairing IL-23-induced Th17 effector response in humans. Psoriasis vulgaris is a chronic, debilitating skin disease that affects millions of people worldwide. The pathophysiological relevance of these findings has been supported by genetic studies that identified polymorphisms in genes associated with NF B activation, IL-23 signaling and T helper 17 (Th17)-cell adaptive immune responses, and in genes associated with the epidermal barrier. This gene encodes an anti-inflammatory innate immune cytokine in the IL-1 family, and implicates the innate immune system in this systemic presentation of psoriasis. Furthermore, rapid suppression of IL-23 and the Th17 cell axis preceded downregulation of IFN -associated genes, which correlated with final disease resolution (Zaba et al.

Psoriasis is an immune-mediated, genetic disease manifesting in the skin or joints or both. Understanding the role of immune function in psoriasis and the interplay between the innate and adaptive immune system has helped to manage this complex disease, which affects patients far beyond the skin. Interleukin-23/Th17 axis. ERDR1; psoriasis; inflammatory skin diseases; Th17; CCR6; CCL20. The pathogenesis of psoriasis is a complex inflammatory process caused by the cytokine axis. IL-6, and IL-23, are significantly increased in psoriatic lesional skin 8. Psoriasis is a chronic and immune-mediated inflammatory skin disorder associated with complex genetic susceptibility. Studies focused on the immunological mechanism have revealed innate and adaptive immune activation in psoriatic lesions, including large numbers of immune cells activated to produce many cytokines, chemokines, and other inflammatory molecules. Knowledge on the genetic basis of psoriasis highlights genetic susceptibility factors that play a crucial role in regulation of immunity, epidermal proliferation, and skin barrier formation.

A Specific Molecular Signature For Psoriasis And Eczema

KEYWORDS: IL-23 axis  innate immunity  psoriasis  skin barrier  Th17 3Keywords: psoriasis, autoimmunity, immunosuppression. Psoriasis is a prevalent, chronic inflammatory skin disease that affects approximately 0. Skin barrier defects play an important role in AD 54. Atopic dermatitis: a disease caused by innate immune defects? Keyword, Author, or DOI GO. Psoriasis is an inflammatory disease affecting the skin, a barrier site. This disease has an incompletely defined etiology and is characterized by dysregulated proliferation and differentiation of keratinocytes, dermal angiogenesis, and immune cell infiltration. Psoriasis is a chronic and immune-mediated inflammatory skin disorder associated with complex genetic susceptibility. Knowledge on the genetic basis of psoriasis highlights genetic susceptibility factors that play a crucial role in regulation of immunity, epidermal proliferation, and skin barrier formation. Keywords. In psoriasis both the innate and adaptive immune system are dysregulated.3 The current pathogenic model in psoriasis highlights the role of T helper 17 (Th 17)/interleukin 17 (IL-17) axis dysfunction as an important source of inflammation. IL-23-activated Th17 cells were discovered to produce IL-17, IL-6 and tumor necrosis factor (TNF) through antigen-specific stimulation. These studies have proved to be a useful biological model and test ground for evaluation of the skin immune system and psoriasis. Phagocytes and dendritic cells (DCs) are the main producers of IL-12 in response to microbial stimulation, 28 and relationship links innate resistance and adaptive immunity.

Psoriasis

Keywords: Th17 cells, Th22 cells, autoimmunity, inflammatory bowel disease, Crohn s disease, ulcerative colitis, asthma, COPD, psoriasis, atopic dermatitis. Th17 cells also produce GM-CSF, another cytokine that promotes enhanced bone marrow production of granulocytes and monocytes, as well as IL-22, a member of the IL-10 cytokine family that acts on epithelial cells of barrier tissues, such as the gut, lung and skin, to enhance anti-microbial defense and epithelial barrier integrity. Keywords GO. (D) As innate immune cells accumulate at the mucosal surface, dendritic cells that have phagocytosed infected, apoptotic neutrophils respond by secreting proinflammatory cytokines that support Th17 differentiation from uncommitted infiltrating CD4+ T cells. A critical role for the IL-23-IL-17 axis in these infectious models is supported by vaccination studies; activation of the Th17 lineage by pertussis toxin and pneumococcal antigen is required to confer full protection against subsequent infection (30, 53, 55). In this model, IL-23 is produced locally in the skin by resident macrophage and dendritic cell (DC) populations that receive a combination of TLR and neuronal signals (15, 17, 18). IL-22 is a cytokine mainly produced by Th17 cells under the control of IL-23.