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

Slides:

Advertisements

Similar presentations

DNA Questions What makes up a DNA backbone? How would you describe how DNA looks? Name the 4 bases that make up DNA. “T” base can only match with? What.

Advertisements

Copyright © 2004 American Medical Association. All rights reserved.

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

Nat. Rev. Nephrol. doi: /nrneph

Figure 3 Example of how a noncoding regulatory rheumatoid

Figure 3 Connexins in cartilage

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.

Nat. Rev. Rheumatol. doi: /nrrheum

Figure 1 Structure of TNF antagonists

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 Heat map of targeted therapies in autoimmune diseases

Nat. Rev. Rheumatol. doi: /nrrheum

Figure 1 Organs involved in coeliac-disease-associated autoimmunity

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

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.

Disease activity over time in autoantibody-positive patients treated with belimumab. Disease activity over time in autoantibody-positive patients treated.

Supplementary Figure 1. Longitudinal study in a representative number of SLE patients one year before (t1), at the time (t2), and one year after renal.

Nat. Rev. Nephrol. doi: /nrneph

Figure 3 Endogenous repair of double-strand DNA breaks

Nat. Rev. Rheumatol. doi: /nrrheum

Figure 4 Approaches to targeting inhibitory immune receptors

Figure 4 Post-test probability as a function of pre-test

Nat. Rev. Rheumatol. doi: /nrrheum

Figure 1 IFA testing for identifying the presence of ANAs

Figure 2 Overlap of associated loci among five rheumatic diseases

Figure 2 Interaction effects between heterozygous HLA‑DRB1

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

Nat. Rev. Rheumatol. doi: /nrrheum

Nat. Rev. Rheumatol. doi: /nrrheum

Nat. Rev. Rheumatol. doi: /nrrheum

Nat. Rev. Rheumatol. doi: /nrrheum

Figure 1 Adaptive immune system of bacteria and archaea

Nat. Rev. Rheumatol. doi: /nrrheum

Nat. Rev. Rheumatol. doi: /nrrheum

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

Figure 1 The current model of the pathogenesis of SLE

Jack C. O’Brien, Benjamin F. Chong

Figure 6 Metabolism of pterins

Figure 1 Principles for the diagnosis and management of osteoarthritis

Nat. Rev. Rheumatol. doi: /nrrheum

Figure 1 The release of DNA from dead and dying cells

Nat. Rev. Rheumatol. doi: /nrrheum

Figure 1 Chronic inflammation and DNA damage in people with SLE

Figure 3 Nuclear-penetrating autoantibodies and synthetic lethality

Figure 1 Overall worldwide prevalence ranges for SLE

Figure 2 Cellular contributions to the development of SLE

Figure 2 Phenotypes of osteoarthritis

Jack C. O’Brien, Benjamin F. Chong

Figure 1 Patterns of joint and organ involvement in rheumatic disease

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

Longitudinal changes in serum G3BP concentrations and SLEDAI in 15 patients with SLE. Each plot represents one patient. Longitudinal changes in serum G3BP.

Celiac disease as a model for SLE

Nat. Rev. Rheumatol. doi: /nrrheum

Presence of autoreactive anti-HLA antibodies among SLE and RA subjects

Figure 2 Involvement of plasmacytoid dendritic cells

Presentation transcript:

Figure 3 The induction of anti-DNA antibodies by bacterial DNA Figure 3 | The induction of anti-DNA antibodies by bacterial DNA. Antibody responses to bacterial DNA differ between individuals with and without systemic lupus erythematosus (SLE). In individuals without SLE, antibodies specific for DNA from certain bacteria are generated. Each antibody binds only to DNA from a particular bacterial species, and none of the antibodies binds to self DNA. This binding pattern indicates specificity for the nucleotide sequence (or for backbone structures dependent on sequence). In at least some patients with SLE, anti-DNA antibodies bind to DNA from different sources, including self DNA. These antibodies bind to backbone determinants and are autoantibodies. Antibodies that bind only to mammalian or self DNA might exist, but are difficult to detect. This scheme suggests that the abnormality in SLE relates to the specificity of antibodies to DNA, rather than to a unique ability to produce antibodies that bind to DNA. Pisetsky, D. S. (2015) Anti-DNA antibodies — quintessential biomarkers of SLE Nat. Rev. Rheumatol. doi:10.1038/nrrheum.2015.151