Figure 3 Transcriptome studies performed in the target

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4. Rheumatologic conditions

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Figure 3 The induction of anti-DNA antibodies by bacterial DNA

Figure 1 Lymphocytes during the disease

Figure 1 Role of innate lymphoid cells (ILCs) in steady state,

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Figure 3 Example of how a noncoding regulatory rheumatoid

Figure 5 Involvement of B cells in SLE

Figure 1 Historical evolution of the clinical classification and

Figure 2 A timeline summarizing the development of diagnostic tools in rheumatology Figure 2 | A timeline summarizing the development of diagnostic tools.

Figure 1 Rheumatoid arthritis development over time in relation to the level of inflammation Figure 1 | Rheumatoid arthritis development over time in relation.

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Figure 1 Induction of immune tolerance

Figure 4 Ex vivo synovial tissue culture viability

Figure 2 Heat map of targeted therapies in autoimmune diseases

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Figure 1 Organs involved in coeliac-disease-associated autoimmunity

Figure 2 Targeted versus untargeted metabolomics approaches

Figure 1 Metabolic profiling as a tool for studying rheumatic diseases

Figure 4 Antinuclear antibodies and disease activity in SLE

Figure 2 Shared genetic loci in systemic autoimmune diseases

Figure 7 Defects in apoptosis

Figure 3 Nucleic acid sensors in SLE

Figure 1 Location of HLA variants known to be associated

Time between systemic lupus erythematosus (SLE) and haematological malignancy diagnoses. Time between systemic lupus erythematosus (SLE) and haematological.

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Figure 3 Strategies to achieve therapeutic inhibition of IL-1

Figure 4 Approaches to targeting inhibitory immune receptors

Figure 2 Overlap of associated loci among five rheumatic diseases

Figure 2 Interaction effects between heterozygous HLA‑DRB1

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Figure 2 Microbiota and osteoimmunology

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Figure 6 Lack of IRF5 causes a reduction in neutrophil influx

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Figure 3 Multi-hit model for autoimmune diseases

Main fields of interest.

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Figure 1 Treat to target, remission and low disease activity in SLE

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Figure 1 The current model of the pathogenesis of SLE

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Figure 1 Reproductive health in patients with rheumatic diseases

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Figure 1 Chronic inflammation and DNA damage in people with SLE

Figure 2 Cellular contributions to the development of SLE

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Figure 1 Patterns of joint and organ involvement in rheumatic disease

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Figure 1 The role of macrophages in RA

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Performance characteristics for multivariate assay SLE panel.

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Figure 3 Transcriptome studies performed in the target tissues of autoimmune rheumatic diseases and the groupings obtained Figure 3 | Transcriptome studies performed in the target tissues of autoimmune rheumatic diseases and the groupings obtained. Various studies have attempted to stratify patients with either systemic sclerosis (SSc)75, lupus nephritis80, rheumatoid arthritis (RA)78,81 or systemic lupus erythematosus (SLE)81 into subgroups using transcriptomic data obtained from samples from various tissue sources. These studies demonstrated clear differences between different subgroups of patients with the same disease diagnosis in the levels of expression of groups of genes associated with particular functions, suggesting different molecular mechanisms behind the same clinical diagnoses. These groups of genes, and their corresponding expression levels in patient subgroups (high, low or medium), are displayed. These patterns are very informative in terms of highlighting the complexity and heterogeneity of autoimmune diseases. Some of these patterns were not replicated in blood samples, diminishing their usefulness for diagnostic purposes. ECM, extracellular matrix. Barturen, G. et al. (2018) Moving towards a molecular taxonomy of autoimmune rheumatic diseases Nat. Rev. Rheumatol. doi:10.1038/nrrheum.2017.220