Open AccessInduction of a pharmacologically active clonotypic B cell response directed to an immunogenic region of the human β 2 ‐adrenergic receptor
Author(s) -
GUILLET JG.,
LENGAGNE R.,
MAGNUSSON Y.,
TATE K.,
STROSBERG A. D.,
HOEBEKE J.
Publication year - 1992
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.1992.tb06981.x
Subject(s) - epitope , immunology , immunogenicity , biology , receptor , autoantibody , immune system , antibody , context (archaeology) , molecular mimicry , biochemistry , paleontology
SUMMARY It has been reported that autoantibodies against the β 2 ‐adrenergic receptors are involved in the pathology of allergic disorders and of Chagas' disease. Therefore, the immune response against a peptide (H26Q) corresponding to the putative second extracellular loop of the human β 2 ‐adrenergic receptor, which could be a target for autoantibody attack, was analysed in view of its possible immunogenicity. The free peptide induced a T cell‐mediated humoral response in the context of three different murine MHC haplotypes. The T cell epitope was found to be localized in the N‐terminal region of the peptide. Highly specific T helper cells were capable of stimulating B cells with the potential to generate a large antibody repertoire reactive with the loop peptide. MoAbs were screened to analyse this B cell response for antibodies potentially interfering with receptor function and a MoAb was found that impaired ligand binding to the receptor.