Skip to main content
. 2022 Oct 19;13:1004232. doi: 10.3389/fimmu.2022.1004232

Table 4.

Key genes with innate immune memory in MRL/lpr mice.

Gene symbol Full name Details
Irf7 interferons regulatory factor7 Apoptosis, cancer, host defense, viral latency, and immunological response are a few of the processes regulated by this protein, which is mostly present in B - cell, plasmacytoid dcs (PDCs), and monocytes. It is also essential for type I IFN-mediated intrinsic immunity (30). Regulation of IRF7 expression and IRF7-mediated immune processes play important roles in SLE (31).
Stat1 signal transducer and activator of transcription 1 Transcription factors, signal transducers and transcription activators of the STAT family, play key roles in immune responses and IFN signaling pathways, regulating various cellular processes (32).
Rsad2 radical S-adenosyl methionine domain containing 2 Type I IFN-mediated viral inhibitory protein, widely involved in antiviral activity. Some studies have found that the expression of methylated RSAD2 in naive CD4+ T cells of SLE patients is significantly increased, and the methylation of the RSAD2 gene CpG site is related to the production of SLE-related autoantibodies (33).
Eif2ak2 eukaryotic translation initiation factor 2-alpha kinase 2 Also known as protein kinase R (PKR), responsible for the regulation of protein synthesis by phosphorylating the translation initiation factor eIF2α of serine-51, the eIF2α kinase PKR can regulate both global and specific mRNA translation in response to a variety of different stimuli, in particular in the immune response (34). EIF2AK2 selectively regulates immune responses and transcription of SLE-related histone genes (35).
Usp18 ubiquitin specific peptidase 18 Cellular activities such as signal transduction, stress responses and the response to pathogenic microbes all rely on this protein. SLE development may be aided by USP18 altering transcribed mRNA degradation and commencement of translation (36).
Isg15 ISG15 ubiquitin-like modifier Ubiquitin-like proteins, either through their coupling to target proteins (ISGylation) or through their role as free or unbound proteins, changes the adaptive immune system to viral infection have a critical role (37).
Ddx58 DEAD/H box helicase 58 Also known as retinoic-acid-inducible gene I (RIG-I). A 925-residue cytoplasmic viral RNA receptor, also a member of the RIG-I-like receptor (RLR) family, is an essential intracellular sensor for several viruses that elicits antiviral IFN responses by recognizing viral double-stranded RNA (dsRNA), whose persistent abnormal activation can cause autoimmune diseases (38).
Ifit1 interferon-induced protein with tetratricopeptide repeats 1 Interferon-induced antiviral RNA-binding protein that specifically binds to single-stranded RNA containing a 5’-triphosphate group (PPP-RNA), thereby acting as a sensor for viral single-stranded RNA and inhibiting the expression of viral messenger RNA. IFIT1 is the first gene identified as a potential pathogenic factor for SLE (39).
Uba7 ubiquitin-like modifier activating enzyme 7 A specific E1-like ubiquitin-activating enzyme involved in ISG15 coupling and acts as an antiviral (40).
Ifit3 interferon-induced protein with tetratricopeptide repeats 3 IFN-induced antiviral protein that acts as an inhibitor of cellular and viral processes, cell migration, proliferation, signaling and viral replication. IFIT3 is one of the genes responsible for the overactive cGAS/STING signaling pathway in human SLE monocytes (41).
Ifi44 interferon-induced protein 44 It is an interferon-inducible gene involved in various biological effects of interferon signaling, such as antiviral. IFI44 is considered a key biomarker in lupus nephritis (LN) (42).
Ifih1 interferon induced with helicase C domain 1 Also known as melanoma differentiation-associated protein 5 (MDA5), the innate immune receptor, which acts as a cytoplasmic sensor of viral nucleic acids, plays a major role in sensing viral infection and activating a range of antiviral responses. IFIH1 may contribute to SLE pathogenesis by altering inflammatory mechanisms (43).