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Hormones as Immune Modulating Agents
Published in Thomas F. Kresina, Immune Modulating Agents, 2020
Production of IFN-γ by murine spleen cells and by human peripheral blood mono-nuclear cells is enhanced by prolactin [85,99,122]. Interferon-regulatory factor-1 gene expression and IFN-γ production were induced by PRL in the Nb2 rat lymphoma cell line and in T lymphocytes. Growth hormone enhanced the production of IL-2 by human lymphocytes and IL-1, tumor necrosis factor-α (TNFα), and superoxide anion production by monocytes [51,72,123] (Table 2). Others found that GH activated monocytes for superoxide production, but not for TNF production, cell adherence, or killing of Mycobacterium tuberculosis [116]. Growth hormone increased the release of IFN-γ from murine splenocytes stimulated with enterotoxin A, whereas the release of IL-1α was inhibited. Prolactin also decreased the release of IL-1α but did not affect IFN-γ release under these conditions [124], Growth hormone treatment of cows reduced the plasma levels of TNFα, cortisol, thromboxane B2, and thromboxane/prostacyclin ratios in response to endotoxin injection [125].
Sjögren Syndrome
Published in Dongyou Liu, Handbook of Tumor Syndromes, 2020
The IRF5 (interferon regulatory factor 5) gene encodes a transcription factor that mediates type I interferon responses in monocytes, dendritic cells, and B cells upon viral infection, leading to the transcription of interferon-α genes and the production of proinflammatory cytokines (e.g., IL-12, p40, IL-6, and TNFα). IRF5 (possibly in association with the neighboring gene TNPO3 s) represents an established risk locus in systemic lupus erythematosus (SLE), rheumatoid arthritis, ulcerative colitis, primary biliary cirrhosis, and systemic sclerosis (SSc). Among known IRF5 pathogenic variants, a CGGGG indel polymorphism in the promoter region is strongly linked to Sjögren syndrome [5].
Neurological manifestations of West Nile virus
Published in Avindra Nath, Joseph R. Berger, Clinical Neurovirology, 2020
Daniel E. Smith, J. David Beckham, Daniel M. Pastula, Kenneth L. Tyler
The innate immune system has a major role in the human host defense against WNV infection. As an overview, the innate immune system is activated by the presence of pathogen-associated molecular patterns (PAMPs) that are detected by pattern recognition receptors (PRRs), which are in host cells. This leads to downstream signaling with effects on NF-kB and interferon regulatory factors, ultimately leading to transcription and release of type 1 interferon, inflammatory cytokines, and chemokines such as TNF-a, IL-1, and CX-CL10 [15,16]. Activation of these pathways acts to restrict viral replication and control tissue tropism, as well as to modulate the adaptive immune response. Production of pro-inflammatory cytokines likely help to control local replication of virus but may also lead to enhanced permeability of the blood–brain barrier which can facilitate neuroinvasion.
Sleep disruption induces activation of inflammation and heightens risk for infectious disease: Role of impairments in thermoregulation and elevated ambient temperature
Published in Temperature, 2023
This multi-cell response shows a close interplay between the innate and adaptive immune system, and this response is tightly regulated by stimulatory signals (e.g. proinflammatory cytokines), and inhibitory signals (e.g. anti-inflammatory cytokines). Moreover, in the case of an intracellular pathogen such as a virus, transcription factors such as interferon regulatory factors are activated, which induce antiviral immune response genes such as type I interferon leading to the translation of interferon (IFN) and activation of Signal Transducer and Activator of Transcription (STAT)-1 and further production of proinflammatory cytokines [67]. Regulation of this response is critical, thereby averting an inadequate immune response or immune deficiency or one that is too robust resulting in host damage such as autoimmunity or septic shock.
Dual role of ARPC1B in regulating the network between tumor-associated macrophages and tumor cells in glioblastoma
Published in OncoImmunology, 2022
Tianqi Liu, Chen Zhu, Xin Chen, Jianqi Wu, Gefei Guan, Cunyi Zou, Shuai Shen, Ling Chen, Peng Cheng, Wen Cheng, Anhua Wu
The interferon regulatory factor (IRF) proteins family were the crucial factors in immunoregulation, cell proliferation regulation and cellular response which was involved in tumorigenesis.46,47 Database analysis predicted IRF2, a member of the interferon regulatory factor (IRF) family, as a TF of ARPC1B, which was confirmed to regulate IFNγ-stimulated ARPC1B expression. Western blotting showed that IRF2 deficiency blocked the upregulation of ARPC1B caused by IFNγ treatment, suggesting that IRF2 also plays an oncogenic role in glioma progression. Several studies indicated the potential oncogenic roles of IFNγ through enrichment of IRF2.48 Moreover, IRF2 was associated with a more advanced pathological grade and worse outcomes in glioma patients.49 These results point to a role of IRF2 not only in the IFNγ-mediated regulation of ARPC1B expression but also in glioma progression.
Cytokine release syndrome in COVID-19: a major mechanism of morbidity and mortality
Published in International Reviews of Immunology, 2022
Yifan Que, Chao Hu, Kun Wan, Peng Hu, Runsheng Wang, Jiang Luo, Tianzhi Li, Rongyu Ping, Qinyong Hu, Yu Sun, Xudong Wu, Lei Tu, Yingzhen Du, Christopher Chang, Guogang Xu
A delayed type 1 IFN response has been proposed as a mechanism for the development of CRS. This is believed to be similar to the case of SARS and MERS [32–34] (Figure 2). RIG-I-like receptors (RLRs) or toll-like receptors (TLRs) recognize viral RNA and the caspase activation recruitment domains of RLRs combined with adapter mitochondrial antiviral signaling protein (MAVS), which recruits TANK-binding kinase 1 (TBK1) and inducible IκB kinase (IKKi). Interferon regulatory factor 3/7(IRF3/7) is phosphorylated by TBK1 and IKKi and further activates the expression of IFN-α/β, which induces the production of IFN-stimulated genes (ISGs) via the JAK-STAT pathway to counter the virus [35]. Coronavirus has been reported to antagonize IFN production and signaling by evading recognition by PRRs, inhibiting RIG-1 or TLRs signaling or blocking IRF3 activation. A recent study showed that expression of open reading frame 6 (ORF6) inhibited RLRs, MAVS and IRF3 through its C-terminus to limit IFN activation and the subsequent interferon-stimulated response element, ISG56 and STAT signal to delay IFN response in the early stages [35]. Low levels of IFN and high levels of proinflammatory cytokines and chemokines are significant characteristics of a delayed IFN response. Monocyte-derived macrophages and DCs respond to viral infection early and release inflammatory cytokines, while the production of IFN-by plasmacytoid dendritic cells is delayed [34].