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Oncolytic Viruses and Histone Deacetylase Inhibitors
Published in Satya Prakash Gupta, Cancer-Causing Viruses and Their Inhibitors, 2014
Vaishali M. Patil, Satya P. Gupta
One possible mechanism by which HDIs act as oncolytics is in downregulation of the cellular antiviral response. Some studies highlighted the involvement of deacetylation in regulating the early interferon response. When the effects of TSA on NF-κB and IRF activity were evaluated, it prevented induction of interferon regulatory factor (IRF) genes without affecting translocation of IRF3 to the nucleus and DNA-binding activity. TSA concludes requirement of HDIs’ activity to initiate transcription from IFN-β promoter (Nusinzon and Horvath 2006). The antiviral response may be regulated by STAT signaling through acetylation and deacetylation (Tang et al. 2007). In the case of virus infection as well as treatment with IFNαt, there is a decrease in IFNα, ISG15 (ubiquitin-like modifier), and ISG54 (interferon-stimulated gene 54) activity, and impaired interferon-stimulated gene factor 3 (ISGF3) complex formation and interferon regulatory factor 7 (IRF7) activation were sustained (Genin et al. 2003; Cheng et al. 2004).
Next-generation immunotherapy for solid tumors: combination immunotherapy with crosstalk blockade of TGFβ and PD-1/PD-L1
Published in Expert Opinion on Investigational Drugs, 2022
Hue Tu Quach, Zhaohua Hou, Rebecca Y. Bellis, Jasmeen K. Saini, Alfredo Amador-Molina, Prasad S. Adusumilli, Yuquan Xiong
Both cancerous cells and pathogens exploit pathways to escape T-cell–mediated immune responses by PD-1 expression [16]. So far, as many as 10 transcription factors and chaperones have validated involvement in Pdcd1 promoter, including transcription factors that are both acute – nuclear factor of activated T cells 1 (NFATc1) [17], activator protein 1 (AP-1) [18], Notch [19], T-box expressed in T cells (T-bet) [20], B lymphocyte-induced maturation protein-1 (Blimp-1) [21], nuclear factor kappa light chain enhancer of activated B cells (NF-κB) [22], B-cell lymphoma (Bcl6) [23] – and chronic – Forkhead box protein O1 (FoxO1) [24], signal transducer and activator of transcription (STAT)3, STAT4, interferon-stimulated gene factor 3 (ISGF3) [25]. Tumor-intrinsic PD-L1 expression is induced by interferons (IFNs) [26], including type I and II IFNs, TNFα, and γ-chain cytokines [27]. Upon antigen exposure, PD-1 induction is linked to prolonged T-cell receptor (TCR) stimulation.
Single nucleotide polymorphisms rs12979860 and rs8099917 in IL-28B and spontaneous clearance of hepatitis C genotype 4
Published in British Journal of Biomedical Science, 2020
AR Youssef, SS Hamam, RM Elkholy
Hepatitis C virus (HCV) is associated with liver disease worldwide, an estimated 170 million are infected. The majority of the infected patients develop chronic liver disorders that range from fibrosis, and cirrhosis to hepatocellular carcinoma. Genotype 4 is the main form of HCV in Africa and Middle East, and around 25% of the infected patients clear the virus spontaneously within 24 weeks without treatment as defined by undetectable level of HCV RNA in plasma. The mechanism of spontaneous eradication depends on the host immune response mainly through the interferon-mediated pathway [1–3]. Among cytokines involved in the antiviral pathway through interferon is interleukin-28 (IL-28), which has two isoforms: IL-28A and IL-28B. IL-28 has been shown to play a role in the adaptive immune response against viruses through induction of two proteins 2ʹ,5ʹ-oligoadenylate synthetase and ISGF3G Interferon Stimulated Gene Factor 3 [4]. The variation of the host immune responses affects the clearance of the viruses and the genetic polymorphism of cytokines has a vital role. Several studies have reported that single nucleotide polymorphisms (SNP) of IL-28 B have an effect on the response of HCV to therapy [5,6]. A recent study linked SNPs in IL-28B (rs12979860) with cirrhosis, fibrosis and hepatocellular carcinoma [7]. We hypothesized differences in SNPS for IL-28B at two sites (rs12979860 and rs8099917) can distinguish active infection from the spontaneous clearance of HCV.