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Myositis
Published in Jason Liebowitz, Philip Seo, David Hellmann, Michael Zeide, Clinical Innovation in Rheumatology, 2023
On the other hand, there is increasing evidence for the role of interferons in DM pathogenesis. Studies have shown an upregulation of the interferon pathway, upregulation of mRNA transcripts induced by interferon type I in the affected muscle,14, 15 overexpression in the muscle of proteins induced by IFN (like myxovirus resistance protein A16, 17), and a strong correlation between type 1 IFN pathway signature biomarker in blood and muscle and skin damage, with INF-b being the driver of this pathological process.57–59
Mental Health and Healthy Aging – Prevention and Management
Published in Goh Cheng Soon, Gerard Bodeker, Kishan Kariippanon, Healthy Ageing in Asia, 2022
While there is evidence for a strong antiviral defense system in the brain vasculature which, in concert with the endothelium’s ability to sense circulating interferon type I signals, would limit SARS-CoV-2 entry into the brain, research is now showing that COVID-19 is more correctly viewed as a vascular disease that attacks the endothelium, impairing its ability to limit SARS-CoV-2 entry into the brain (Lei et al., 2021). This has implications for the elderly, who are already disposed to vascular and neurological vulnerability. A Lancet report on how mental healthcare should change as a consequence of the COVID-19 pandemic has noted that elderly people are at especially high risk of severe COVID-19 illness and mental-health-related consequences because they might already have some cognitive decline (Moreno et al., 2020).
T Cells
Published in Miroslav Holub, Immunology of Nude Mice, 2020
The NK populations were obviously responsible for interferon production upon cocultivation of the virus-infected cell line with nude mouse spleen cells.84 In vivo, only heavy irradiation or pretreatment with anti-mouse interferon (type I) could break the NK barrier of the nudes and induce invasiveness and metastases even of the virus-infected tumor cell lines.84
Case Fatality Rate and Severity of COVID-19 among Patients with Sickle Cell Disease: A Systematic Review and Meta-Analysis
Published in Hemoglobin, 2023
Tarcísio Silva Borborema, Julio Cesar Moreira Brito, Edleusa Marques Lima Batista, Rodrigo Siqueira Batista
In addition, the development of COVID-19 associated with ACS usually leads to an increase in the release of cytokines that cause airway inflammation [53,54]. This event could be an important additional risk factor for COVID-19 case fatality rate in SCD patients. Inflammation, particularly in the lower respiratory tract, may certainly play a role in increasing susceptibility to the virus and even the intensity of the inflammatory storm that frequently occurs in fatal COVID-19 [55]. Moreover, the enhanced inflammatory response triggered by ACS has been associated with a severely impaired interferon type I (IFN-I) response characterized by low production and activity of this natural antiviral component [56]. The type I IFN response (including IFN-α and IFN-ᵝ) represents the major first line of defense against viruses. Indeed, type I IFN activates a powerful antiviral defense program with hundreds of interferon-stimulated genes that can disrupt all steps of viral replication [57,58]. Therefore, a reduced type I IFN signature in SCD patients who have ACS could be a hallmark of severe COVID-19 susceptibility in this patient population [59].
The molecular structure and biological functions of RNA methylation, with special emphasis on the roles of RNA methylation in autoimmune diseases
Published in Critical Reviews in Clinical Laboratory Sciences, 2022
Wanwan Zhou, Xiao Wang, Jun Chang, Chenglong Cheng, Chenggui Miao
The transfer of mRNAs from the nucleus to the cytoplasm is an important step in the translation of mRNAs in the cytoplasm. RNA methylation also affects this mechanism. RNA methylation, especially m6A and m5C, is crucial in the process of mRNA nuclear export. DEAD-box (DDX) 46 inhibits the production of interferon type I (IFN-I) after viral infection. DDX46 recruits ALKBH5 through the DEAD helicase domain of DDX46 to demethylate the m6A modified IFN-I transcripts. Demethylation enhances the retention of IFN-I transcripts in the nucleus, thus preventing their translation and production [69]. During the murine leukemia virus life cycle, m5C is installed in the viral RNA transcript in the nucleus. The m5C modified sites are recognized by the ALYREF reader, which helps their export to the cytoplasm. In tRNA, m5C stabilizes the RNA structure, reducing cleavage by nucleases in cells [70]. The absence of RNA methylation leads to the disruption of mRNA nuclear export and affects subsequent gene expression [71].
The immunology of SARS-CoV-2 infection, the potential antibody based treatments and vaccination strategies
Published in Expert Review of Anti-infective Therapy, 2021
Zahra Payandeh, Niloufar Mohammadkhani, Mohsen Nabi Afjadi, Saeed Khalili, Masoumeh Rajabibazl, Zahra Houjaghani, Masoomeh Dadkhah
Effective innate immune response against the viral infection is correlated to interferon type I (IFN1) and its downstream pathway controlling viral replication and induction of effective adaptive immune response [43]. The PAMPs of RNA viruses not only are recognized by either the endosomal RNA receptors or TLR3 but also identified by TLR7 or the cytosolic RNA sensor (RIG-I/MDA5). Involvement of these molecules could lead to activation of the downstream signaling cascade of NF-κB and IRF3 accompanied by their nuclear translocation and finally IFN1expression [28,43,44]. Type I IFN activates the JAK-STAT pathway via IFNAR and JAK1/TYK2 kinases phosphorylate STAT1/STAT2. The STAT1/2 complexes with IRF9 and induces the nuclear transcription of IFN-stimulated genes (ISGs) which are under the control of promoters containing IFN-stimulated response element (ISRE) [28].