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Critical Reviews™ in Immunology
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ISSN Imprimir: 1040-8401
ISSN En Línea: 2162-6472

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Critical Reviews™ in Immunology

DOI: 10.1615/CritRevImmunol.v27.i3.30
pages 221-232

PART I. Peptide Immunotherapy
Natural and Autoantibodies to Human T-Cell Receptor Vβ Segments: Potential Roles in Immunomodulation

Miranda K. Adelman
Arizona Arthritis Center, University of Arizona, Tucson, AZ 85724, USA
Samuel F. Schluter
Department of Immunobiology, University of Arizona, Tucson, AZ 85724, USA
Ian F. Robey
Arizona Cancer Center; Microbiology and Immunology, College of Medicine, University of Arizona, Tucson, AZ 85724
John J. Marchalonis
Department of Immunobiology, University of Arizona College of Medicine P.O. Box 24-5049 Tucson, AZ 85724

SINOPSIS

Although the manifestation of inflammatory autodestructive disease is the result of major immunological dysfunction, recent evidence indicates that the immune system attempts to compensate by the production of immunomodulatory autoantibodies. Healthy humans have low levels of naturally occurring autoantibodies directed against the first complementarity-determining region (CDR1) and third framework region (FR3) of their own T-cell receptor (TCR) Vβ segments, but individuals suffering from rheumatoid arthritis (RA) or systemic lupus erythematosus (SLE) can have highly elevated levels of these autoantibodies. We cloned and characterized human anti-TCR monoclonal autoantibodies (mAAbs) from RA and SLE patients. Because of the cross-reactions between distinct CDR1 segments of human TCR Vβ and corresponding murine homologs, it was possible to show that human mAAbs blocked the capacity of a murine TH1 cell line (DO11.10) to produce IL-2 in response to antigenic stimulation in vitro. These results support the hypothesis that autoantibodies against TCR Vβ can shut down TH1-mediated inflammatory autodestructive reactions.


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