Nat. Rev. Rheumatol. doi: /nrrheum

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The Complement System Andrew E Thompson MD FRCPC Fellow in Rheumatology University of British Columbia.

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The Complement System Andrew E Thompson MD FRCPC

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

Figure 2 Cell-mediated disease mechanisms of lupus nephritis

Nat. Rev. Rheumatol. doi: /nrrheum

Figure 3 Example of how a noncoding regulatory rheumatoid

Figure 3 Connexins in cartilage

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Figure 1 Structure of TNF antagonists

Figure 1 Induction of immune tolerance

Figure 3 Methods to detect trough levels of therapeutic antibodies

Figure 2 Assays for detecting antidrug antibodies to TNF inhibitors

Figure 3 Proposed mechanisms underlying the links

Nat. Rev. Rheumatol. doi: /nrrheum

Figure 2 Targeted versus untargeted metabolomics approaches

Figure 1 Metabolic profiling as a tool for studying rheumatic diseases

Figure 1 Targets for monoclonal antibodies in B-cell lineages

Nat. Rev. Rheumatol. doi: /nrrheum

Figure 4 Antinuclear antibodies and disease activity in SLE

Figure 3 Transcriptome studies performed in the target

Figure 1 Location of HLA variants known to be associated

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Figure 3 TNFSF activities enhancing immune cell activation

Topics Type I hypersensitivity Type II hypersensitivity 18-1.

Nat. Rev. Rheumatol. doi: /nrrheum

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Figure 4 Approaches to targeting inhibitory immune receptors

Figure 1 Activation and signalling of IL-1

Figure 2 Prevention of antigen–antibody

Figure 2 Cas9 targeting using crRNA (CRISPR

Figure 2 Interaction effects between heterozygous HLA‑DRB1

Nat. Rev. Rheumatol. doi: /nrrheum

Figure 3 Statistical approaches for the analysis of metabolomic data

Nat. Rev. Rheumatol. doi: /nrrheum

Figure 2 Influence of fucosylation on IgG effector functions

Figure 2 Emerging models of antibody-mediated rejection (ABMR) and

Figure 3 Multi-hit model for autoimmune diseases

Nat. Rev. Rheumatol. doi: /nrrheum

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Figure 1 Neuromuscular junction in myasthenia gravis (MG)

Figure 3 LDL autoimmunity in atherosclerosis

Nat. Rev. Rheumatol. doi: /nrrheum

Figure 3 Current model of immunopathogenesis in CIDP

Nat. Rev. Rheumatol. doi: /nrrheum

Autoimmunity through Cytokine-Induced Dendritic Cell Activation

Figure 1 The current model of the pathogenesis of SLE

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Figure 1 Chronic inflammation and DNA damage in people with SLE

Figure 3 Nuclear-penetrating autoantibodies and synthetic lethality

Figure 2 Cellular contributions to the development of SLE

Lecture 14 Antibody-Antigen Reactions

Figure 4 Role of chemokines in dendritic cell migration

Figure 1 Extrinsic and intrinsic pathways of apoptosis

Figure 1 The role of macrophages in RA

Figure 2 The main effects of adipokines on bone remodelling in osteoarthritis Figure 2 | The main effects of adipokines on bone remodelling in osteoarthritis.

Receiver operating curve of soluble C3, C4, antibodies to double-stranded DNA (anti-dsDNA) compared with complement C4d levels on erythrocytes (EC4d) and.

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Complement and antibody abnormalities at baseline and relation to disease activity clinical SELENA-SLEDAI (A) and PGA scores (B) in relation to the presence.

Nat. Rev. Rheumatol. doi: /nrrheum

A schematic presentation of secreted, endocytic, and signaling pattern-recognition receptors. A schematic presentation of secreted, endocytic, and signaling.

Figure 2 Involvement of plasmacytoid dendritic cells

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Nat. Rev. Rheumatol. doi:10.1038/nrrheum.2017.107 Figure 2 Strategies for detecting or eliminating autoreactive B cells and/or autoantibodies Figure 2 | Strategies for detecting or eliminating autoreactive B cells and/or autoantibodies. a | Autoreactive B cells can be detected using biotinylated autoepitope peptides that are tetramerized with fluorescently-labelled avidin; in this manner, autoreactive B cells can be purified and enriched from peripheral blood. These cells can also be selectively depleted using nanoparticles coated with an autoepitope peptide and a complement-activating peptide. The complement-activating peptide initiates the complement cascade to lyse the autoreactive B cell (complement-mediated cytoxicity). Autoreactive B cells can be silenced with autoepitope peptides coupled to anti-Fcγ receptor IIb (FcγRIIb) antibodies. In this scenario, the peptide–antibody complex crosslinks the B cell receptor (BCR) and FcγRIIb, silencing the B cell. b | Autoreactive plasma cells can be detected using affinity matrix technology in which both the secreted autoantibodies and the plasma cell bind to a matrix made up of F(ab)2 fragments of antibodies reactive towards the plasma cell marker CD138 coupled with autoepitope peptides. The marked cell is subsequently killed by the complement system. Autoantibodies can be cleared using an antigen-based heteropolymer system. In this system, an anti-complement receptor 1 (CR1) antibody is linked to a double stranded DNA (dsDNA) motif. Anti-dsDNA autoantibodies are cleared from the peripheral blood by binding to CR1‑expressing red blood cells. Abetimus sodium, a tetramerized double-stranded oligodeoxyribonucleotide attached to a carrier platform, can also clear anti-dsDNA autoantibodies. Pozsgay, J. et al. (2017) Antigen-specific immunotherapies in rheumatic diseases Nat. Rev. Rheumatol. doi:10.1038/nrrheum.2017.107