Clinical & Experimental Allergy

Absence of functional inhibition of cloned human β2-adrenergic receptors by autoantibodies in asthmatic subjects

Authors

  • P. C. POTTER,

    Corresponding author
    1. Department of Clinical Science and Immunology and MRC Cell Biology Unit, University of Cape Town and Groote Schuur Hospital, Medical School, Observatory, South Africa
      Dr P. C. Potter, Department of Clinical Science and Immunology, University of Cape Town and Groote Schuur Hospital, Medical School, Observatory 7925, South Africa.
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  • L. VAN WYK,

    1. Department of Clinical Science and Immunology and MRC Cell Biology Unit, University of Cape Town and Groote Schuur Hospital, Medical School, Observatory, South Africa
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  • D. WHITE,

    1. Department of Clinical Science and Immunology and MRC Cell Biology Unit, University of Cape Town and Groote Schuur Hospital, Medical School, Observatory, South Africa
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  • B. S. DAKERS,

    1. Department of Clinical Science and Immunology and MRC Cell Biology Unit, University of Cape Town and Groote Schuur Hospital, Medical School, Observatory, South Africa
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  • F. Z. CHUNG,

    1. Department of Clinical Science and Immunology and MRC Cell Biology Unit, University of Cape Town and Groote Schuur Hospital, Medical School, Observatory, South Africa
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  • E. B. DOWDLE

    1. Department of Clinical Science and Immunology and MRC Cell Biology Unit, University of Cape Town and Groote Schuur Hospital, Medical School, Observatory, South Africa
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Dr P. C. Potter, Department of Clinical Science and Immunology, University of Cape Town and Groote Schuur Hospital, Medical School, Observatory 7925, South Africa.

Summary

Using guinea-pig lung membranes and cloned human β2-receptor adrenergic receptors the effects of whole serum, plasma, purified immunoglobulins and cellular activation products on β2-adrenergic receptor ligand binding and function were investigated. Sera from 24 non-asthmatic subjects and 115 asthmatics in different clinical categories were studied. There were no significant differences between antagonist ([125I] cyanopindolol) inhibition mediated by serum, plasma or by purified IgG when the asthmatics were compared with non-asthmatics. There was also no inhibition of 10−6m isoproterenol stimulated cAMP release from L cells expressing human β2-adrenergic receptors, by plasma, DEAE purified IgG fractions from asthmatics and non-asthmatics, or by products of activated platelets or lymphocytes. Since we have no evidence that immunoglobulins from asthmatic subjects exert functional inhibition of human β2-adrenergic receptors we conlcude that autoantibodies to the β2-adrenergic receptors do not play an important functional role in the pathophysiology of asthma.

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