caa a22 4500 475743865 CHVBK 20180406123507.0 cr unu---uuuuu 170329e20000101xx s 000 0 eng 10.1023/A:1007086608036 doi (NATIONALLICENCE)springer-10.1023/A:1007086608036 Production and Characterization of Monoclonal IgM Autoantibodies Specific for the T-Cell Receptor [Elektronische Daten] [Ian Robey, Samuel Schluter, David Yocum, John Marchalonis] Natural autoantibodies to the T-cell receptor (Tcr) have been identified in all human sera. However, titer, epitope specificity, and isotype vary with physiological conditions, autoimmune diseases, and retroviral infections. The levels of anti-Tcr autoantibodies in rheumatoid arthritis (RA) patients are significantly higher than in normal individuals, and the autoantibodies are typically IgM. To obtain detailed information on these autoantibodies, we generated B-cell heterohybridomas secreting monoclonal IgM autoantibodies (mAAbs) from the synovial tissue and peripheral blood of RA patients. We selected clones secreting mAAbs that bound a major Vβ epitope defined by a synthetic peptide that contains the CDR1 region of the Vβ 8.1 gene product. From these we isolated a subset of seven mAAbs that bound a recombinant single-chain Vα/Vβ construct containing the peptide epitope and, also to JURKAT cells which express Vβ 8.1. The mAAbs produced by these clones were distinct from each other in their V-region sequences. However, all the V regions were essentially identical to germline sequences in both the heavy and light chains. Heavy-chain CDR3 segments ranged in length from 17 to 26 residues, did not correspond to any known autoantibodies, and showed extensive N-region diversity in the V(D)J junctions. Five monoclonal autoantibodies use VH 3 genes, while the remaining two utilized VH 4 sequences. Light-chain variable regions used were Vκ 3 (two), Vλ 3 (four), and one Vλ 2. These autoantibodies derived their unique features from their CDR3 segments that could not be aligned with any known sequences. Plenum Publishing Corporation, 2000 Autoantibodies nationallicence rheumatoid arthritis nationallicence T-cell receptor nationallicence IgM nationallicence CDR3 region nationallicence Robey Ian Department of Microbiology and Immunology, College of Medicine, University of Arizona, 85724, Tucson, Arizona aut Schluter Samuel Department of Microbiology and Immunology, College of Medicine, University of Arizona, 85724, Tucson, Arizona aut Yocum David Arizona Arthritis Center, College of Medicine, University of Arizona, 85724, Tucson, Arizona aut Marchalonis John Department of Microbiology and Immunology, College of Medicine, University of Arizona, 85724, Tucson, Arizona aut Journal of Protein Chemistry Kluwer Academic Publishers-Plenum Publishers 19/1(2000-01-01), 9-21 0277-8033 19:1<9 2000 19 10930 https://doi.org/10.1023/A:1007086608036 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1023/A:1007086608036 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Robey Ian Department of Microbiology and Immunology, College of Medicine, University of Arizona, 85724, Tucson, Arizona aut NATIONALLICENCE 700 1- Schluter Samuel Department of Microbiology and Immunology, College of Medicine, University of Arizona, 85724, Tucson, Arizona aut NATIONALLICENCE 700 1- Yocum David Arizona Arthritis Center, College of Medicine, University of Arizona, 85724, Tucson, Arizona aut NATIONALLICENCE 700 1- Marchalonis John Department of Microbiology and Immunology, College of Medicine, University of Arizona, 85724, Tucson, Arizona aut NATIONALLICENCE 773 0- Journal of Protein Chemistry Kluwer Academic Publishers-Plenum Publishers 19/1(2000-01-01), 9-21 0277-8033 19:1<9 2000 19 10930 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer