|
|
||||||||
From the Department of Microbiology and Medicine, The Johns Hopkins University, and the O'Neill Laboratories of The Good Samaritan Hospital, Baltimore, Maryland 21212
Abstract
The cell-bound IgE molecules on basophil granulocytes were enumerated by C1 fixation transfer technique. The average number of IgE molecules per basophil granulocyte was 10,000 to 40,000. The number did not have direct correlation with serum IgE level; however, a rough inverse relationship was observed between the number of cell-bound IgE molecules and the optimal concentration of anti-IgE for maximum histamine release from the cells. The results suggested that the number and affinity of cell-bound IgE antibody molecules probably determine the sensitivity of basophils to allergen.
When leukocytes were incubated with 100 µg to 1 mg/ml of E myeloma protein, the number of basophil-bound IgE molecules significantly increased. The number of receptor sites for IgE molecules per basophils was estimated to be between 30,000 and 100,000. IgE molecules have high affinity for the receptor but the binding of the molecules with the receptor is reversible. The association constant of the binding reaction was estimated to be on the order of 108 to 109. Basophils from all normal individuals studied combined IgE molecules upon incubation with E myeloma protein. After sensitization with a reaginic serum, however, the leukocytes from some of these donors failed to release histamine upon challenge with antigen under the usual experimental condition. These cells previously termed "non-acceptor" cells, released histamine if they were challenged in the presence of D2O, which enhanced biochemical processes after the antigen-antibody reaction. The results indicated that even such "non-acceptor" cells combined IgE antibody upon passive sensitization with reaginic serum and, therefore, that failure of antigen-induced histamine release from these cells was not due to lack of IgE antibody on their surface.
Footnotes
1 The work was supported by Research Grant AI 10060 from the United States Public Health Service. This paper is Publication No. 73 from the O'Neill Laboratories at The Good Samaritan Hospital.
This article has been cited by other articles:
![]() |
L. A. Youssef, M. Schuyler, L. Gilmartin, G. Pickett, J. D. J. Bard, C. A. Tarleton, T. Archibeque, C. Qualls, B. S. Wilson, and J. M. Oliver Histamine Release from the Basophils of Control and Asthmatic Subjects and a Comparison of Gene Expression between "Releaser" and "Nonreleaser" Basophils J. Immunol., April 1, 2007; 178(7): 4584 - 4594. [Abstract] [Full Text] [PDF] |
||||
![]() |
C. L. Kepley, L. Youssef, R. P. Andrews, B. S. Wilson, and J. M. Oliver Multiple Defects in Fc{epsilon}RI Signaling in Syk-Deficient Nonreleaser Basophils and IL-3-Induced Recovery of Syk Expression and Secretion J. Immunol., November 15, 2000; 165(10): 5913 - 5920. [Abstract] [Full Text] [PDF] |
||||
![]() |
D. MacGlashan Jr, J. McKenzie-White, K. Chichester, B. S. Bochner, F. M. Davis, J. T. Schroeder, and L. M. Lichtenstein In Vitro Regulation of Fc&b.epsi;RIalpha Expression on Human Basophils by IgE Antibody Blood, March 1, 1998; 91(5): 1633 - 1643. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. Hamburger Peptide inhibition of the Prausnitz-Kustner reaction Science, August 1, 1975; 189(4200): 389 - 390. [Abstract] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |