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Enhancement of Human Eosinophil Complement Receptors by Pharmacologic Mediators
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Abstract
Human eosinophils and neutrophils were shown to have receptors for rabbit and human IgG, and for the human complement components C4, C3b, and C3d (A. R. E. Anwar and A. B. Kay (1977), J. Immunol. 119: 976, 1977. We now report that agents which have a selective effect on human eosinophil motility in vitro, such as the ECF-A peptides and histamine, also enhance the number of receptors for C3b and C4, but not for IgG and C3d. The ECF-A tetrapeptides (Val-Gly-Ser-Glu and Ala-Gly-Ser-Glu) and histamine increased the percentage of eosinophils forming rosettes with EAC3b by approximately 90%, an effect that was observed in a dose- and time-dependent fashion. Neutrophil and monocyte C3b receptors were unaltered by this treatment and other pharmacologic agents such as bradykinin and the prostaglandins E1, E2, and F2α were without effect on any of the cell types when tested in the dose range 10-4 to 10- mole/1. 5-hydroxytryptamine enhanced C3b receptors by 25% at a dose of 10-4 mole/liter. The ECF-A tetrapeptides and histamine also enhanced C4 receptors, but under the same experimental conditions C3d receptors were unaffected. A major histamine catabolite, imidazole acetic acid, also shown to induce preferentially human eosinophil locomotion (L. W. Turnbull and A. B. Kay (1976), Immunology, 31, 797), had a comparable effect on eosinophil C3b receptors whereas histidine and other major histamine catabolites including N-acetyl histamine, methyl histamine and 1-methyl-4-imidazole acetic acid had no receptor enhancing activity. These studies suggest that agents which have a preferential effect on human eosinophil locomotion also alter their membrane receptors for C3b and C4 so raising the possibility that these pharmacologic mediators of hypersensitivity may regulate certain eosinophil-dependent biologic reactions.
Title: Enhancement of Human Eosinophil Complement Receptors by Pharmacologic Mediators
Description:
Abstract
Human eosinophils and neutrophils were shown to have receptors for rabbit and human IgG, and for the human complement components C4, C3b, and C3d (A.
R.
E.
Anwar and A.
B.
Kay (1977), J.
Immunol.
119: 976, 1977.
We now report that agents which have a selective effect on human eosinophil motility in vitro, such as the ECF-A peptides and histamine, also enhance the number of receptors for C3b and C4, but not for IgG and C3d.
The ECF-A tetrapeptides (Val-Gly-Ser-Glu and Ala-Gly-Ser-Glu) and histamine increased the percentage of eosinophils forming rosettes with EAC3b by approximately 90%, an effect that was observed in a dose- and time-dependent fashion.
Neutrophil and monocyte C3b receptors were unaltered by this treatment and other pharmacologic agents such as bradykinin and the prostaglandins E1, E2, and F2α were without effect on any of the cell types when tested in the dose range 10-4 to 10- mole/1.
5-hydroxytryptamine enhanced C3b receptors by 25% at a dose of 10-4 mole/liter.
The ECF-A tetrapeptides and histamine also enhanced C4 receptors, but under the same experimental conditions C3d receptors were unaffected.
A major histamine catabolite, imidazole acetic acid, also shown to induce preferentially human eosinophil locomotion (L.
W.
Turnbull and A.
B.
Kay (1976), Immunology, 31, 797), had a comparable effect on eosinophil C3b receptors whereas histidine and other major histamine catabolites including N-acetyl histamine, methyl histamine and 1-methyl-4-imidazole acetic acid had no receptor enhancing activity.
These studies suggest that agents which have a preferential effect on human eosinophil locomotion also alter their membrane receptors for C3b and C4 so raising the possibility that these pharmacologic mediators of hypersensitivity may regulate certain eosinophil-dependent biologic reactions.
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