IL-12 and IL-23 are closely related in structure, and have been shown to play crucial roles in regulation of immune responses. However, little is known about the regulation of these cytokines in T cells. Here, we investigated the roles of PI3K and MAPK pathways in IL-12 and IL-23 production in human Jurkat T cells in response to Toxoplasma gondii and LPS. IL-12 and IL-23 production was significantly increased in T cells after stimulation with T. gondii or LPS. T. gondii and LPS increased the phosphorylation of AKT, ERK1/2, p38 MAPK, and JNK1/2 in T cells from 10 min post-stimulation, and peaked at 30-60 min. Inhibition of the PI3K pathway reduced IL-12 and IL-23 production in T. gondii-infected cells, but increased in LPS-stimulated cells. IL-12 and IL-23 production was significantly reduced by ERK1/2 and p38 MAPK inhibitors in T. gondii- and LPS-stimulated cells, but not in cells treated with a JNK1/2 inhibitor. Collectively, IL-12 and IL-23 production was positively regulated by PI3K and JNK1/2 in T. gondii-infected Jurkat cells, but negatively regulated in LPS-stimulated cells. And ERK1/2 and p38 MAPK positively regulated IL-12 and IL-23 production in Jurkat T cells. These data indicate that T. gondii and LPS induced IL-12 and IL-23 production in Jurkat T cells through the regulation of the PI3K and MAPK pathways; however, the mechanism underlying the stimulation of IL-12 and IL-23 production by T. gondii in Jurkat T cells is different from that of LPS.
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http://dx.doi.org/10.3347/kjp.2017.55.6.613 | DOI Listing |
Int J Mol Sci
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Department of Internal Medicine, Angiology and Physical Medicine, Center for Laser Diagnostics and Therapy, Medical University of Silesia in Katowice, Batorego 15 Street, 41-902 Bytom, Poland.
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January 2025
Division of Musculoskeletal and Dermatological Sciences, School of Biological Sciences, The University of Manchester, Manchester, UK.
Background: The current management of psoriasis does not differentiate between young and old patients in selecting the safest and/or most effective biologic.
Objectives: To explore the effect of age at treatment initiation in response to biologics in patients with moderate-to-severe psoriasis in the UK and Eire.
Methods: Data from patients registering to the British Association of Dermatologists Biologics and Immunomodulators Register (BADBIR) from 2007-2024 on first course of Tumour Necrosis Factor (TNF), interleukin (IL) 12/13, IL-17 and IL-23 inhibitors (i) with at least 6 months' follow-up were included.
Inn Med (Heidelb)
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Abteilung für interventionelle gastroenterologische Endoskopie, Klinik für Gastroenterologie und Hepatologie, Universitätsklinikum Essen, Essen, Deutschland.
Background: In chronic inflammatory bowel diseases (IBD), severe flares are characterized by intense inflammatory activity and a high disease burden for patients. Treatment addresses both short-term goals (e.g.
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Department of Dermatology, Asahikawa Medical University, Asahikawa, JPN.
Eczematous paradoxical reactions are commonly associated with anti-interleukin-17A (anti-IL-17A) antibodies. However, IL-23 p19 inhibitors can also cause similar cutaneous manifestations. We present a case of a 77-year-old Japanese woman with palmoplantar pustulosis (PPP), who developed eczematous lesions on her face, neck, and dorsum of the hands 10 weeks after initiating guselkumab treatment.
View Article and Find Full Text PDFNutrients
December 2024
Department of Dermatology, Heersink School of Medicine, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Background/objective: Ultraviolet (UV) B radiation leads to DNA damage by generating cyclobutane pyrimidine dimers (CPDs). UVB-induced CPDs can also result in immune suppression, which is a major risk factor for non-melanoma skin cancer (NMSC). UVB-induced CPDs are repaired by nucleotide repair mechanisms (NER) mediated by xeroderma pigmentosum complementation group A (XPA).
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