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The Inducible Defense System: The Induction and Development of the Inducible Defence
Published in Julius P. Kreier, Infection, Resistance, and Immunity, 2022
Michael A. Hickey, Diane Wallace Taylor
As noted above, macrophages can be activated by contact with cytokine, bacterial compounds, and components of the complement cascade. They can also be activated by direct contact with activated T helper cells. In this interaction, the CD40L on the activated T helper cell binds to CD40 which is constitutively expressed on monocytes and macrophages (Figure 8.10). This interaction, plus a second signal activates macrophages. As noted above, activated macrophages are more efficient in killing both intracellular pathogens (e.g., the bacteria that cause tuberculosis and leprosy) and extracellar bacteria than are resting macrophages. Thus, the Th1 cell greatly enhances the cellular immune response.
Cytokines, Apoptosis, and Immune Therapy in HIV Infection
Published in Thomas F. Kresina, Immune Modulating Agents, 2020
Jerôme Estaquier, Jean-Claude Ameisen
It has been shown that Th1 and Th2 cytokines regulate the Th1/Th2 cell expansion by exerting two different effects. On one hand, cytokines such as IL-2 and IL-4 induce the expansion of the Th1 and the Th2 CD4 T cell population. On the other hand, cytokines that can be secreted by accessory cells play an indirect role in Th1 and Th2 expansion by down-regulating the converse Th cell population. The Th2 cytokine IL-10 inhibits Th1 cell expansion while the Th1 cytokine 7 interferon inhibits Th2 cell expansion [92]. Cytokine-mediated regulation of the Th1/Th2 cell ratio also operates through the control of programmed T cell death induction. Cytokine-mediated programmed Th1 cell death may represent a general mechanism of Th1 cell down-regulation (Figure 1). Among cytokines secreted by accessory cells, IL-12 and IL-10 may play an essential role in controlling the decision of CD4 Th cells to expand or to die. The local environment may fail to provide the costimulatory signals required for CD4 Th1 cell survival and lead to programmed Th1 cell death. Understanding how cytokines involved in the regulation of Th1/Th2 responses control T cell survival and T cell death may have important implications for the therapeutic approach of immunosuppression associated with chronic infectious diseases.
Adaptive immune response: Antigens, lymphocytes, and accessory cells
Published in Gabriel Virella, Medical Immunology, 2019
Gabriel Virella, John W. Sleasman
Signals mediated by interleukins include those mediated by interleukin-1 (IL-1) and interleukin-12 (IL-12). Interleukin-1 is a cytokine that promotes growth and differentiation of many cell types, including T and B lymphocytes. Both membrane-bound and soluble IL-1 are important in activating T lymphocytes in vitro. Membrane-bound IL-1 can only activate T lymphocytes in close contact with the APC. Interleukin-12 (IL-12) promotes Th1 cell differentiation as previously mentioned. However, all these costimulatory signals are not specific for any given antigen. The specificity of the immune response is derived from the essential and first activation signal delivered through the antigen-specific TCR.
Long Non Coding RNA FOXD3‑AS1 Alleviates Allergic Rhinitis by Elevating the Th1/Th2 Ratio via the Regulation of Dendritic Cells
Published in Immunological Investigations, 2023
Hao Zhang, Xinhua Zhu, Hongbing Liu, Chunping Yang, Yuehui Liu
Th1/Th2 cell imbalance is the pathophysiological basis of a series of inflammatory reactions (Moss et al. 2005). After Th1 cells differentiate, the transcription factor T-bet is highly expressed, and the cytokine IFN-γ is secreted, forming a positive feedback loop; however, after Th2 cells differentiate, the transcription factor GATA-3 is highly expressed, and the cytokine IL-4 is secreted, also forming a positive feedback loop. A large number of inflammatory cells and cytokines further trigger IgE synthesis and induce allergic reactions such as basophilic granulocyte and mast cell degranulation (Lin et al. 2016). Our previous study revealed that lncRNA FOXD3-AS1 markedly inhibited Th2-type immunoreactions in CD4+ T cells cultured with LPS-treated nasal epithelial cells (NECs) (Zhang et al. 2020). Here, our work further demonstrated that LV-FOXD3-AS1 significantly reduced Th2 cells in the peripheral blood of AR model mice but had no significant effects on Th1 cells, resulting in an increase in the Th1/Th2 ratio. In addition, LV-FOXD3-AS1 also reversed the significant alterations in the levels of the Th1/Th2 cell-related cytokines IL-4, IL-5, IL-13, IL-6, and IFN-γ in the peripheral blood of AR model mice. However, the specific mechanisms by which LV-FOXD3-AS1 affected the Th1/Th2 ratio in AR model mice were not clear.
Docetaxel-induced acute myositis: a case report with review of literature
Published in Journal of Chemotherapy, 2021
Sariya Wongsaengsak, Miguel Quirch, Somedeb Ball, Anita Sultan, Nusrat Jahan, Mohamed Elmassry, Shabnam Rehman
Even though the clinical and histopathological findings could help to distinguish between different types of inflammatory myopathy as discussed above, but the precise mechanisms leading to tissue injury in each type are still poorly defined.23 The immune related mechanism is commonly used to explain the pathogenesis in most hypotheses.23 Several studies demonstrated that multiple cytokines could induce an infiltration of immune cells into the muscle tissue.24 The key mediator of pathogenesis in these diseases was found to be the overexpression of interferon gamma (IFN-ˠ), tumor necrosis factor (TNF), and interleukin (IL)-12 in the blood and muscle tissue of patients. This finding implicated that the T helper type 1 (Th1) cell, the primary source of these cytokines could be a prominent driver of the disease process.25
Interferon gamma/interleukin-4 modulation, anti-inflammatory and antioxidant effects of hesperidin in complete Freund’s adjuvant (CFA)-induced arthritis model of rats
Published in Immunopharmacology and Immunotoxicology, 2020
Stephen Adeniyi Adefegha, Nathieli Bianchin Bottari, Daniela Bitencourt Leal, Cínthia Melazzo de Andrade, Maria Rosa Schetinger
During inflammatory process, the CD4+ T helper (Th) cells are activated to release particular cytokines in the microenvironment thus aiding the development of RA [5,6]. These naive CD4+ T cells are polarized into lineages of Th cells, including Th1, Th2, Th17, and regulatory T cells (Treg), which are defined by their individual cytokine production patterns and function [7]. Th1 cells are pro‐inflammatory and secrete interferon (IFN‐γ), which promote the inflammatory process and joint damage, while Th2 cell‐derived agent such as IL‐4 induce humoral immunity [8]. Oxidative stress has a prominent role in the etiology and pathogenesis of joint tissue injury and chronic inflammation in patients with RA, which may lead to connective tissue degradation and joint and periarticular deformities [9].