| Original language | English (US) |
|---|---|
| Pages (from-to) | 962-968 |
| Number of pages | 7 |
| Journal | The Journal of Allergy and Clinical Immunology |
| Volume | 78 |
| Issue number | 5 PART 2 |
| DOIs | |
| State | Published - Nov 1986 |
| Externally published | Yes |
Bibliographical note
Funding Information:The “atopic state”‘. * represents an inherited symptom complex consisting of allergic rhinitis, asthma, and atopic dermatitis. Several immune and inflammatory functions in atopic individuals differ from those in nonatopic individuals. IgE antibody responsest o antigen are the classic means of distinguishing allergic from nonallergic individuals.’ Allergic individuals have higher total serum IgE levels and higher numbers of IgE receptors per basophil than have normal individuals4 Only allergic individuals make IgE an- tibody responsest o antigens such as pollen-associateda n-tigens. At least two genes, one regulating total IgE and one regulating immune responses,a re thought to be responsible for these IgE responses.’ Because IgE responsesa re regulated by suppressorc ells,5 it has been postulated that atopic From the Division of Clinical Immunology, Department of Medi-cine, Johns Hopkins University School of Medicine at the Good Samaritan Hospital, Baltimore, Md. Supported by grants AI 02790, AI 08270, and AI 12810 from the National Institutes of Health. Publication No. 623 of the O’Neill Research Laboratory of the Good Samaritan Hospital, Baltimore, Md. Reprint requests: Marshall Plaut. M.D., Division of Clinical Im-munology, Department of Medicine, Johns Hopkins University School of Medicinea t the Goed SamaritanH ospital,5 601L och Raven Blvd., Baltimore, MD 21239.