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Introduction/Background

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Figure 1 Lymphocytes during the disease

Nat. Rev. Rheumatol. doi: /nrrheum

of different experimental arthritis models

Figure 3 The adaptive and maladaptive energy matrices

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

Figure 1 Grip strength across the lifecourse

Nat. Rev. Rheumatol. doi: /nrrheum

Nat. Rev. Rheumatol. doi: /nrrheum

Nat. Rev. Rheumatol. doi: /nrrheum

Nat. Rev. Rheumatol. doi: /nrrheum

Figure 1 Induction of immune tolerance

Figure 3 Methods to detect trough levels of therapeutic antibodies

Figure 2 Risk factors for sarcopenia

Figure 2 Systemic immune responses to cryptococcal antigen

Figure 4 Simplified T cell and antigen presenting

Figure 3 Proposed mechanisms underlying the links

Figure 2 Heat map of targeted therapies in autoimmune diseases

Nat. Rev. Rheumatol. doi: /nrrheum

Figure 5 Defects in the JAK–STAT signalling pathway

Figure 2 Main functions of IL-1

Figure 3 The T-cell cytokine tree in IBD

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 3 Transcriptome studies performed in the target

Figure 2 Shared genetic loci in systemic autoimmune diseases

Figure 7 Defects in apoptosis

Figure 3 Nucleic acid sensors in SLE

Nat. Rev. Rheumatol. doi: /nrrheum

Figure 1 Location of HLA variants known to be associated

Figure 4 Proinflammatory immune cells and their crosstalk in patients with IBD Figure 4 | Proinflammatory immune cells and their crosstalk in patients.

Figure 3 Strategies to achieve therapeutic inhibition of IL-1

Nat. Rev. Rheumatol. doi: /nrrheum

Figure 2 Type 3 immunity and AS

Nat. Rev. Rheumatol. doi: /nrrheum

Figure 2 Microbiota and osteoimmunology

Figure 3 Statistical approaches for the analysis of metabolomic data

Figure 6 Lack of IRF5 causes a reduction in neutrophil influx

Nat. Rev. Rheumatol. doi: /nrrheum

Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro

Nat. Rev. Rheumatol. doi: /nrrheum

Figure 3 Effect of sialylated glycoforms on IgG activity

Figure 3 Multi-hit model for autoimmune diseases

Immunopathogenesis of Rheumatoid Arthritis

Nat. Rev. Clin. Oncol. doi: /nrclinonc

Nat. Rev. Rheumatol. doi: /nrrheum

Nat. Rev. Rheumatol. doi: /nrrheum

Nat. Rev. Rheumatol. doi: /nrrheum

Nat. Rev. Rheumatol. doi: /nrrheum

Nat. Rev. Rheumatol. doi: /nrrheum

Figure 2 Emerging hallmarks of T cells in rheumatoid arthritis

Figure 1 Overview of biosimilar product development

Figure 3 Current model of immunopathogenesis in CIDP

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

Figure 1 The current model of the pathogenesis of SLE

Figure 8 HRQOL in individuals with RA

Figure 6 Metabolism of pterins

Figure 1 Reproductive health in patients with rheumatic diseases

Nat. Rev. Rheumatol. doi: /nrrheum

Nat. Rev. Rheumatol. doi: /nrrheum

Figure 2 Biologics that target CD4+ T helper (TH)-cell subsets

Figure 2 Embryonic origins of tissue-resident macrophages

Figure 1 Chronic inflammation and DNA damage in people with SLE

Figure 2 Phenotypes of osteoarthritis

Nat. Rev. Rheumatol. doi: /nrrheum

Figure 1 Patterns of joint and organ involvement in rheumatic disease

Figure 4 Role of chemokines in dendritic cell migration

Nat. Rev. Rheumatol. doi: /nrrheum

Figure 1 The role of macrophages in RA

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Nat. Rev. Rheumatol. doi:10.1038/nrrheum.2015.171 Figure 1 Cytokine profiles that subserve the biology of discrete phases of the rheumatoid arthritis disease process Figure 1 | Cytokine profiles that subserve the biology of discrete phases of the rheumatoid arthritis disease process. This figure depicts the notion that groups of cytokines (e.g. IL-6, IL-21, IL-23, IL-17) likely drive adaptive immune activation/differentiation and loss of tolerance in preclinical or early arthritis, whereas distinct profiles might dominate the transition to chronicity or the maintenance of established disease (e.g. TNF, IL-6), and perhaps phases of disease dominated by response to damage (e.g. cytokines released by activators of damage-sensing pathways). Such cytokine profiles could yield new biomarker profiles, or novel insights into the rational, 'pathogenesis stage-dependent' application of cytokine-targeting therapeutics. For example, cytokine signatures could separate those patients destined to fail (A) or respond to (B) a given intervention, and once in remission those patients destined to flare (C) or remain in a low disease activity state (D). McInnes, I. B. et al. (2015) Cytokines in rheumatoid arthritis — shaping the immunological landscape Nat. Rev. Rheumatol. doi:10.1038/nrrheum.2015.171