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The role of S.aureus and L.plantarum as an immunomodulator of IFNα macrophages and fibronectin dermal fibroblast secretion
Published in Robert Hofstra, Noriyuki Koibuchi, Suthat Fucharoen, Advances in Biomolecular Medicine, 2017
R.S.P. Saktiadi, S. Sudigdoadi, T.H. Madjid, E. Sutedja, R.D. Juansah, T.P. Wikayani, N. Qomarilla, T.Y. Siswanti
In this study, increasing dosages of SA exposure to macrophages cell culture caused the increase of IFNα in proportion to the increase of dosage. The highest levels of interferon was yielded by an exposure of high dosage SA, 51.40 pg/dL. This espoused the findings of some similar researches on the modulation of immune system due to S.aureus colonization, by CpG molecules to be recognized particularly by TLR2, which then induces the productions of proinflammation cytokines such as TNFα, IL6 by macrophages through MyD88-dependent signaling pathways that stimulates IRF7 (IFN-regulatory factor-7) and finally induces IFNα pathways.(Pascolini et al. 2011).
Human Herpesvirus Type 8/Kaposi Sarcoma Herpesvirus
Published in Satya Prakash Gupta, Cancer-Causing Viruses and Their Inhibitors, 2014
Hiba El Hajj, Raghida Abou Merhi, Ali Bazarbachi
Another latent protein, LANA-2, also known as viral interferon regulatory factor 3 (vIRF3), is expressed in the nuclei of virtually all HHV-8-infected lymphoid cells in primary effusion lymphoma (PEL) and in the majority of HHV-8-infected cells in multicentric Castleman’s disease (MCD) but not in KS (Cunningham et al. 2003). LANA-2 is expressed during latency and antagonizes p53-mediated apoptosis in vitro (Wies et al. 2008). It stimulates c-Myc function (Lubyova et al. 2007) and stabilizes HIF-1α and pro-apoptotic cellular interferon regulatory factor-5 (IRF-5) (Shin et al. 2008). It was shown that it stimulates growth inhibition via G2/M cell cycle arrest (Table 10.2) (Bi et al. 2011). LANA-2 was also shown to directly interact with cellular IRF-3, IRF-7, and the transcriptional co-activator CBP/p300, and to stimulate their transcriptional activity, leading to enhanced expression of type I interferon and chemokine genes (Lubyova et al. 2004).
Neurovirulence of the West Nile Virus
Published in Sunit K. Singh, Daniel Růžek, Neuroviral Infections, 2013
Besides up-regulating various ISG with antiviral properties, type I IFN produced strongly augments its own production by establishing a positive feedback loop. Binding of type I IFN to IFN-α/βR up-regulates both IRF-1 and IRF-7 to further enhance the production of type I IFN (Marié et al. 1998; Sato et al. 1998 b; Lin et al. 2000; Zhou et al. 2000). This establishes a strongly antiviral state to further inhibit viral progression. The importance of type I IFN in limiting viral infection was demonstrated in mice lacking the IFN-α/βR. Besides enhanced viremia and elevated viral titers in both the brain and peripheral organs, these mice had increased mortality after WNV infection (Samuel and Diamond 2005). Treatment of cells with type I IFN has been shown to reduce viral titer and inhibit cytopathicity (Anderson and Rahal 2002; Samuel and Diamond 2005).
Chicken toll-like receptors and their significance in immune response and disease resistance
Published in International Reviews of Immunology, 2019
Aamir Nawab, Lilong An, Jiang Wu, Guanghui Li, Wenchao Liu, Yi Zhao, Qimin Wu, Mei Xiao
In avian species, it has been postulated that chTLR4 regulates only MyD88 independent pathways [73]. The studies have suggested this as the possible reason that the chicken genome lacks TRAM ortholog, which plays a role of the bridge in recruiting TRIF to the initiated chTLR-4 [74–76]. But several other studies illuminate that the chTLR4 signaling pathway is activated by both MyD88 dependent and independent mechanism, however the reason behind this phenomenon is still unknown [76]. In MyD-88-independent pathway and/or TRIF-dependent signaling pathway [77], TIR domain binds with TRIF, which is crucial for recruitment of RIP1 (receptor interacting protein kinase 1) and TRAF6 adaptor molecules to activate TAK1, which overall result in activation of NF-kB, such as in the MyD88 mediated dependent pathway [1, 72, 78]. On the other hand, TRIF associate with TRAF3 and TANK-binding kinase 1 (TBK1-IKK complexes). These complexes induce phosphorylation and cause activation of IRF3 and IRF7 [1, 72], which produces pro-inflammatory cytokines [1]. A study has reported that viral infection (dsRNA) activate by IRF3 [70, 72]. Hence, chTLR3 signaling pathway also triggers IRF3 and produces IFN-β in MyD88 independent manner. Therefore, both chTLR3 and chTLR4 use the MyD88 independent mechanism to produce IFN-β [70, 72].
Signalling pathways identified in salivary glands from primary Sjögren’s syndrome patients reveal enhanced adipose tissue development
Published in Autoimmunity, 2018
Lara A. Aqrawi, Janicke Liaaen Jensen, Gunnvor Øijordsbakken, Ann-Kristin Ruus, Ståle Nygård, Marit Holden, Roland Jonsson, Hilde Kanli Galtung, Kathrine Skarstein
Microarray analysis conducted on SG from 6 pSS patients and 6 non-SS controls revealed signalling pathways contributing to adipose tissue development and reduced mitochondrial fatty acid beta-oxidation in the target organ of pSS (Figure 1). The genes contributing to these mechanisms were highlighted in gene set A (blue annotation). Interestingly, genes involved in interferon production and signalling were also detected (gene set B, purple annotation), and upregulated in pSS patients. These comprised of interferon regulatory factor (IRF)-1, IRF7, and IRF9. Another distinct feature observed when accounting for all the signalling pathways expressed in the microarray analysis was the upregulation of IL6, IL10, and IL17 genes as a consequence of activated immune responses in the SG of pSS patients. An overview of these overexpressed genes and their function is listed in Table 2.
Repolarizing heterogeneous leukemia-associated macrophages with more M1 characteristics eliminates their pro-leukemic effects
Published in OncoImmunology, 2018
Xiao Yang, Wenli Feng, Rong Wang, Feifei Yang, Lina Wang, Shayan Chen, Yongxin Ru, Tao Cheng, Guoguang Zheng
To investigate the roles of IRF7 on macrophages, RAW264.7 cells were infected with blank MSCV-GFP retrovirus or retrovirus carrying IRF7 (Fig S5B). After cell sorting, stably transfected cell lines, verified by RT-PCR (Fig. 6A) and Western blot (Fig S5C), were named RAW-V, RAW-IRF7, respectively. RAW-IRF7 expressed higher level of M1-associated genes (iNOS, TNFa and IL-6) but lower level of M2-realated genes (ARG1 and CFS1) than RAW-V (Fig. 6A). Furthermore, LPS stimulated the expression of iNOS, the classical M1 marker, while IL-4 stimulated the expression of ARG1, the classical M2 marker, in RAW-V and RAW-IRF7 in both time-and dose-dependent manners (Fig. 6B, 6C). Notably, only upon LPS stimulation, the increase in RAW-IRF7 was more dramatic than in RAW-V.