ArticleProceedings of the National Academy of Sciences of the United States of America1994
Control of autoantibody affinity by selection against amino acid replacements in the complementarity-determining regions.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- Rheumatoid Factor and Anti-Modified Protein Antibody Reactivities Converge on IgG Epitopes.Arthritis & rheumatology (Hoboken, N.J.) · 2022Article
- Is Tolerance Broken in Autoimmunity?Clinical medicine insights. Pathology · 2017Article
- Identification of a novel stereotypic IGHV4-59/IGHJ5-encoded B-cell receptor subset expressed by various B-cell lymphomas with high affinity rheumatoid factor activity.Haematologica · 2016Article
- Use of similar immunoglobulin VH gene segments by MALT lymphomas of the ocular adnexa.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2009Article
- Effect of 51p1-related gene copy number (V1-69 locus) on production of hepatitis C-associated cryoglobulins.Clinical and experimental immunology · 2001Article
- Cell-cell interactions in synovitis: antigen presenting cells and T cell interaction in rheumatoid arthritis.Arthritis research · 2001Review
- B lymphocyte involvement in ankylosing spondylitis: the heavy chain variable segment gene repertoire of B lymphocytes from germinal center-like foci in the synovial membrane indicates antigen selection.Arthritis research · 2001Article
- Rheumatoid factor isotype switch and somatic mutation variants within rheumatoid arthritis synovium.Immunology · 1999Article
- Rheumatoid factors in primary Sjögren's syndrome (pSS) use diverse VH region genes, the majority of which show no evidence of somatic hypermutation.Clinical and experimental immunology · 1999Article
- Do self-perpetuating B lymphocytes drive human autoimmune disease?Immunology · 1999Review
- Antigen-driven clonal proliferation of B cells within the target tissue of an autoimmune disease. The salivary glands of patients with Sjögren's syndrome.The Journal of clinical investigation · 1998Article
- Antigen-dependent B cell differentiation in the synovial tissue of a patient with reactive arthritis.Molecular medicine (Cambridge, Mass.) · 1997Article
- Peripheral deletion of rheumatoid factor B cells after abortive activation by IgG.Proceedings of the National Academy of Sciences of the United States of America · 1997Article
- Sequence analysis of immunoglobulin variable region genes that encode autoantibodies expressed by lymphomas of mucosa associated lymphoid tissue.Clinical molecular pathology · 1996Article
- VH3-21 B cells escape from a state of tolerance in rheumatoid arthritis and secrete rheumatoid factor.Molecular medicine (Cambridge, Mass.) · 1995Article
- 3rd International Symposium on the Immunotherapy of the Rheumatic Diseases. 10-14 May 1995, Cyprus. Abstracts.Annals of the rheumatic diseases · 1995Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rheumatoid factor (RF) autoantibodies can be produced in healthy individuals after infections or immunizations and thus escape normal tolerization mechanisms. It has not been clear whether such autoantibodies can undergo somatic hypermutation and affinity maturation similar to antibodies to exogenous antigens. We have investigated how these autoantibodies are regulated in normal individuals by analyzing the sequences of monoclonal IgM RFs obtained as hybridomas from donors after immunization. The variable regions undergo extensive hypermutation, but in contrast to antibodies against exogenous antigens, there is a strong selection against mutations that result in replacement of amino acids in the hypervariable, or complementarity-determining, regions. Furthermore, we found no increase in affinity of these RFs with the accumulation of mutations. This suggests that high-affinity variants are tolerized during the hypermutation process and there is a peripheral mechanism operating on certain autoreactive B cells that, while not deleting or anergizing all autoreactive cells, prevents the generation of high-affinity autoantibodies. Comparison of RFs by using the VH1 DP-10 heavy chain variable region segment from both normal individuals and rheumatoid arthritis (RA) patients suggests that RF from RA patients may not be subject to such a controlling mechanism.
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