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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).
Mathematical Modelling of Signalling Networks in Cancer
Published in Inna Kuperstein, Emmanuel Barillot, Computational Systems Biology Approaches in Cancer Research, 2019
Inna Kuperstein, Emmanuel Barillot
As mentioned in the previous section, in a cancer context, the balance between Treg and Th17 phenotypes is of particular interest, as Treg cells are mainly associated with tumour tolerance, while Th17 cells are mainly associated with anti-tumoural response.
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.
Effect of lyophilization and spray-drying on cytokine levels and antioxidant capacity in human milk
Published in Drying Technology, 2022
Vanessa Javera Castanheira Neia, Joana Maira Valentini Zacarias, Josiane Bazzo de Alencar, Patrícia Daniele Silva dos Santos, Christyna Beatriz Genovez Tavares, Meliana G. Paula, Silvio Claudio da Costa, Mariana Maciel de Oliveira, Celso Vataru Nakamura, Oscar Oliveira Santos, Jeane E. L. Visentainer, Jesuí V. Visentainer
The cytokines IL˗17A, IL-17F, IL-21, and IL-22 are produced by Th17 cells and are involved in the activation of neutrophils and increased barrier immunity against extracellular bacteria and fungi.[26] Among Th17 cytokines, IL-21 concentration was higher than IL-17A/F and IL-22, in our study. IL-21 acts on naive B cells and induces antibody isotype switching to IgA.[27] The presence of IgA in HM compensates for the small amount of IgA in the infant,[28] and seems to play a role in regulating the immune response to dietary antigens.[29]
Effects of long-term high-level lead exposure on the immune function of workers
Published in Archives of Environmental & Occupational Health, 2022
Jianrui Dou, Le Zhou, Yi Zhao, Wu Jin, Huanxi Shen, Feng Zhang
Cytokines are small biologically active proteins synthesized by stimulated immune cells such as T-cells, B-cells, and macrophages and non-immune cells (endothelial cells and fibroblasts). They are key mediators of inflammatory responses, affecting the interaction and communication between cells and stimulating them to induce inflammation. T-helper cells can be divided into Th1, Th2, and Th17 cells according to their secreted cytokines and different functions. Th1 cells are primarily involved in cellular immunity and Th2 cells are primarily involved in humoral immunity. The balance between Th1 and Th2 cells is an important link in immune regulation and imbalance disorders can cause immune deficiency. Th1 cells mainly secrete IL-2, IFN-γ, and TNF-α. Th2 cells mainly secrete IL-4, IL-6, and IL-10. The newly discovered Th17 cells are a T-cell subset with its main effector cytokine being IL-17. This cytokine plays an important role in inducing inflammation and autoimmune tissue damage. Dobrakowski et al.20 compared three groups of workers and found that levels of IFN-γ, IL-2 (related to Th1 cells), IL-4 (related to Th2 cells), and IL-17A (related to TH17 cells) did not change after short-term exposure to Pb. However, the levels of IFN-γ, IL-2, IL-4, and IL-17A in workers exposed to Pb for extended periods of time were 82%, 32%, 22%, and 17% higher than those in the control group, respectively. They believed that short-term exposure to Pb did not affect the levels of cytokines or Th1, Th2, and Th17-mediated immune responses, while chronic exposure did. Conversely, Yucsoy et al.21 found that IFN-γ levels (blood lead levels; BLL = 59.35 ± 3.19 μg/dL) of employees of a battery factory exposed to Pb for a long time were lower than those of the control group (BLL = 4.83 ± 0.99 μg/dL). Furthermore, no significant correlation between IL-4 or IFN-γ serum levels was detected in workers of a Korean battery manufacturing industry with blood Pb concentrations >300 μg/L or <300 μg/L.22 In addition, healthy workers exposed to low Pb levels (blood Pb = 91–460 μg/L) presented significantly higher plasma levels of IL-10 and TNF-α when compared to those who were not exposed to Pb (blood Pb = 32–180 μg/L).23 Dyatlov and Lawrence[24] verified that serum levels of IL-6 increased significantly in mice exposed to Pb after being infected with Listeria monocytogenes. In the current study, we detected no significant differences in Thl/Th2/Thl7 cytokine levels between the high-Pb and low-Pb groups. The reason for this may have been that the change in Pb concentrations in the range observed in this study had little effect on cytokine levels. Therefore, the conclusions regarding the effect of Pb on cytokines remain unclear and further studies should allow us to clarify this issue.7