Induction of a pharmacologically active clonotypic B cell response directed to an immunogenic region of the human beta 2-adrenergic receptor.
It has been reported that autoantibodies against the beta 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 beta 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.
Guillet
J G
JG
Laboratory of Molecular Immunopharmacology, CNRS, Paris, France.
Lengagne
R
R
Magnusson
Y
Y
Tate
K
K
Strosberg
A D
AD
Hoebeke
J
J
D000818:Animals; D000911:Antibodies, Monoclonal; D001402:B-Lymphocytes / Q000648:ultrastructure*; D002999:Clone Cells; D000939:Epitopes; D051379:Mice; D008805:Mice, Inbred A; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D011943:Receptors, Adrenergic, beta / Q000276:immunology*
D000911:Antibodies, Monoclonal; D000939:Epitopes; D011943:Receptors, Adrenergic, beta