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Concise Publication Free access | 10.1172/JCI106998
Division of Allergy, Department of Medicine, Children's Hospital Medical Center, Boston, Massachusetts 02115
Division of Immunology, Department of Medicine, Children's Hospital Medical Center, Boston, Massachusetts 02115
Division of Endocrinology, Department of Medicine, Children's Hospital Medical Center, Boston, Massachusetts 02115
Department of Pediatrics, Harvard Medical School, Boston, Massachusetts 02115
Find articles by Colten, H. in: JCI | PubMed | Google Scholar
Division of Allergy, Department of Medicine, Children's Hospital Medical Center, Boston, Massachusetts 02115
Division of Immunology, Department of Medicine, Children's Hospital Medical Center, Boston, Massachusetts 02115
Division of Endocrinology, Department of Medicine, Children's Hospital Medical Center, Boston, Massachusetts 02115
Department of Pediatrics, Harvard Medical School, Boston, Massachusetts 02115
Find articles by Gabbay, K. in: JCI | PubMed | Google Scholar
Published July 1, 1972 - More info
Cytochalasin B, a metabolic product of several fungi, enhances up to 10-fold the sensitivity and reactivity of human leukocytes to antigen E or anti-IgE-mediated histamine release. The effect of cytochalasin B is a result of its action on the second, antigen-independent, stage of histamine release. These data suggest that normally, antigen-triggered histamine release is modulated by a cytochalasin-sensitive barrier (CSB). This CSB modulation of histamine release can be separated from the modulating effect of cyclic adenosine monophosphate (AMP).