Table 1.

Summary of recent transcriptome studies in SLE

Groups	Authors	Year	SLE samples and patients	Material	Method	Summary of findings
Pascual and colleagues	Chiche et al. [17]	2014	157 samples/ 62 adults	Whole blood	Microarray	Modular repertoire analysis identified three distinct IFN signatures in SLE, which involved the previous IFNα signature as well as IFNβ and IFNγ signatures.
	Banchereau et al. [33]	2016	924 samples/ 158 children	Whole blood	Microarray	Longitudinal immunomonitoring stratified SLE patients into seven groups based on five modules correlated with SLEDAI (erythropoiesis, IFN, myeloid lineage/neutrophils, plasmablasts and lymphoid lineage modules).
	Hong et al. [34]	2019	92 pregnant women	Whole blood	Microarray	Sustained IFN response and plasma cell signatures were observed in pregnant SLE patients with fetal complications. Patients with preeclampsia showed remarkable upregulation of the neutrophil signature.
	Nehar-Belaid et al. [22]	2020	33 children and 8 adults	PBMCs	scRNA-seq	The high IFN signature was limited to a small number of cells within each major cell type. Subpopulations enriched in ISGs and/or monogenic lupus-associated genes were expanded, especially in active SLE.
Other groups	McKinney et al. [39]	2015	23 adults	CD4+ T cells, CD8+ T cells	Microarray	The exhaustion signature in CD8+ T cells, which was associated with poor outcomes in patients with viral infections, was correlated with a lower risk of disease relapse in AAV and SLE patients.
	Chong et al. [40]	2015	9 adults with DLE	Skin	Microarray	CD163+ macrophages were polarized in DLE skin. M1 macrophage-associated genes such as CXCL10 and CCL5 were upregulated in DLE skin.
	Sherbiny et al. [18]	2018	114 adults	PBMCs and sorted monocytes, T, NK and three B cell subsets	qRT-PCR	IFN score A was increased in SLE only, whereas IFN score B was increased in both SLE and RA. Both scores were correlated with mucocutaneous and hematological, but not musculoskeletal, activity in SLE.
	Petri et al. [16]	2019	243 adults	Whole blood	Microarray	IFN, BAFF, plasma cell and LDG signatures were relatively stable in patients over time. The changes in IFN and BAFF signatures did not coincide with changes in disease activity.
	Panousis et al. [35]	2019	142 samples/ 142 adults	Whole blood	RNA-seq	The SLE “activity signature” included genes related to immune cell metabolism, protein synthesis and proliferation. Active nephritis was characterized by neutrophil and humoral response signatures.
	Catalina et al. [20]	2019	More than 1000 patients from multiple publicly available datasets	PBMCs, whole blood, skin, synovium, kidney, monocytes, B cells and CD4+ T cells	Microarray	The IFN signature was enriched in SLE skin and synovium and, to a lesser extent, in LN kidneys. The lack of correlation between the IFN signature in PBMCs and SLEDAI is due to its persistent overexpression in inactive SLE monocytes.
	Minstry et al. [37]	2019	11 adults	PBMCs	RNA-seq, scRNA-seq	The highest ISG expression was observed in LDGs among various cell subpopulations. CD10+ LDGs showed the strongest proinflammatory phenotype and the most significant association with organ damage.
Accelerating Medicine Partnership in SLE Network	Der et al. [43]	2017	16 adults (kidney) and 12 adults (skin) with LN	Kidney and skin	scRNA-seq	IFN scores in renal tubular cells were positively correlated with the chronicity index, urinary protein levels and glomerular IgG deposition. Patients with higher IFN scores were less likely to respond to treatment.
	Der et al. [44]	2019	21 adults (kidney) and 17 adults (skin) with LN	Kidney and skin	scRNA-seq	The fibrotic gene signatures related to ECM pathways in tubular cells predicted a poor treatment response. Comparisons among histological subclasses revealed distinct inflammation and fibrosis pathways in each subclass.
	Arazi et al. [45]	2019	21 adults with LN	Kidney	scRNA-seq	CD16+ monocytes acquired phagocytic function and differentiated into M2-like macrophages in the kidney of LN patients. Twenty-one cell subpopulations including cytotoxic CD8+ T cells and DN2-like B cells infiltrated the kidney.
	Fava et al. [46]	2020	30 adults with LN	Kidney and urine	scRNA-seq + proteomics	A chemokine gradient induced by IFNγ distinguished proliferative LN from membranous LN. Urinary chemokines were predominantly produced by infiltrating CD8+ T cells, followed by NK and myeloid cells.

Among the studies cited in the manuscript, the studies published since 2014 are listed

AAV anti-neutrophil cytoplasmic antibodies-associated vasculitis, BAFF B cell activating factor, DLE discoid lupus erythematosus, DN2 double negative memory B cells 2, ECM extracellular matrix, IFN interferon, IgG immunoglobulin G, LDGs low-density granulocytes, LN lupus nephritis, NK natural killer, PBMCs peripheral blood mononuclear cells, qRT-PCR quantitative reverse-transcription polymerase chain reaction, RA rheumatoid arthritis, RNA-seq RNA-sequencing, scRNA-seq single-cell RNA-sequencing, SLE systemic lupus erythematosus, SLEDAI SLE disease activity index