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Immune Responses
Published in Ronald Fayer, Lihua Xiao, Cryptosporidium and Cryptosporidiosis, 2007
Depending on the nature of the antigens that the immune system encounters, CD4+ T helper (Th) cells may induce a cell-mediated immune response (Th1) or antibody-mediated response (Th2). These diverse Th responses are determined by the spectrum of cytokines produced by the T-cells themselves and by the antigen-presenting cells. In a Th1 response, IL-12 produced by dendritic cells and macrophages drives the T-cells to produce IFN-?. This type of response is usually required to control and eliminate intracellular infections. In a Th1 response, CD8+ cytotoxic T-cells may also be induced with or without help from CD4+ T cells. These cells kill infected cells in an MHC class I-restricted fashion. A Th2 response is associated with production of IL-4, IL-5, IL-9, and IL-13, and polarized Th2 responses are observed in allergies and asthma; they may also be required to eliminate helminth infections (Wynn, 2003). The Th1 and Th2 pathways can oppose each other as Th1 responses are inhibited by Th2 cytokines such as IL-4 and IL-13 and, similarly, Th2 development is inhibited by Th1cytokines. Recently, another Th response associated with inflammation has been characterized. Th17 cells are induced by the IL-12-related cytokine IL-23, and they produce IL-17, IL-6, and TNF-a (Weaver et al., 2006). This response occurs in autoimmune diseases, but its involvement in immunity to infection is less clear.
Flavonoids from Quercus Genus: Applications in Melasma and Psoriasis
Published in Tatjana Stevanovic, Chemistry of Lignocellulosics: Current Trends, 2018
Esquivel-García Roberto, Velázquez-Hernández María-Elena, Valentín-Escalera Josué, Valencia-Avilés Eréndira, Rodríguez-Orozco Alain-Raimundo, Martha-Estrella García-Pérez
IL-12 and IL-23, which share a common p40 subunit, constitute an axis of regulation and activation of lymphocytes Th1 and Th17, which are characterized by the production of pro-inflammatory cytokines such as IL-17A, IL-17F, IFN-α and tumor necrosis factor alpha (TNF-α) (Croxford et al. 2014). These cytokines stimulate the production and release of chemokines and adhesion molecules by KCs (CCL20, CXCL1, CXCL2, CXCL8, CXCL9, CXCL10, and CXCL11), facilitating lymphocyte recruitment and infiltration into the psoriatic plaque (Kim and Krueger 2015). Psoriasis is now recognized as a disease mediated by polarized Th17 cells that produce IL-17 which originates a continuous circle responsible for the perpetuation of the disease (Fig. 3) (Harden et al. 2015).
Genetic variants affecting chemical mediated skin immunotoxicity
Published in Journal of Toxicology and Environmental Health, Part B, 2022
Isisdoris Rodrigues de Souza, Patrícia Savio de Araujo-Souza, Daniela Morais Leme
High IL-18 serum levels are associated with psoriasis and AD (Gangemi et al. 2003; Sedimbi, Hägglöf, and Karlsson 2013; Tanaka et al. 2001). Psoriasis is correlated with an overexpression of Th1 cytokines and relative underexpression of Th2 cytokines. IL18 gene expression may play an important role in this disease by inducing Th1 response because IL-18 is a potent inductor of synthesis of IFN- γ, TNF-α and other mediators (Gangemi et al. 2003). Further, IL-18 may recruit DCs expressing IL-18 R to inflammatory areas under Th1 conditions as in psoriatic lesions (Lee, Cho, and Park 2015). When synergized with IL-23, IL-18 promotes development and maintenance of Th17 cells that were also implicated in developing the disease. Results from previous studies indicated that IL-18 serum or plasma levels correlate well with the Psoriasis Area and Severity Index (PASI) (Pietrzak et al. 2003; Takahashi et al. 2010). The expression of IL-18 was also elevated in initially active and progressive plaque-type psoriatic lesions (Companjen et al. 2004). Further, in cooperation with IL-23, IL-18 induced severe inflammation and enhanced psoriasis-like epidermal hyperplasia (Shimoura et al. 2017). Niu et al. (2019) using IL-18 knockout mouse model in imiquimod-induced psoriasis found that IL-18 promoted IL-17 mRNA expression and decreased IL-4 production, which may then prevent Th2 responses.