Involvement of IgE in con A-induced histamine release from human basophils in vitro

Magro, Albert M.

doi:10.1038/249572a0

Cited by 39 publications

(35 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It has been demonstrated that, while soluble Con A stimulates histamine secretion in sensitized mast ceils, it does not do so in unsensitized cells, suggesting that its stimulating activity is due to its binding to surface IgE molecules (20). Consistent with this view is the observation that the binding of monovalent Fab fragments of anti-IgE antibodies to sensitized mast cells inhibits the stimulatory activity of Con A (24).…”

Section: Discussionsupporting

confidence: 68%

Localized mast cell degranulation induced by concanavalin A-sepharose beads. Implications for the Ca2+ hypothesis of stimulus-secretion coupling.

Lawson¹,

Fewtrell²,

Raff³

1978

The Journal of Cell Biology

View full text Add to dashboard Cite

Concanavalin A (Con A) covalently linked to Sepharose 4B beads induced localized degranulation of sensitized rat peritoneal mast cells in regions of contact between beads and cells. This degranulation was Ca2+ dependent and was not seen when sensitized mast cells bound to beads conjugated with a nonstimulating lectin, wheat germ agglutinin, or when unsensitized mast cells bound to Con A-Sepharose. The finding that sensitized mast cells which had adhered to Con A-Sepharose beads degranulated in regions of the cell away from the area of bead contact if exposed to soluble Con A excluded the possibility that the localized release was due to a redistribution of the IgE receptors or putative Ca2+ channels to the region of bead contact. The results suggest that, if an influx of Ca2+ is the mechanism for initiating mast cell degranulation, then the opening of Ca2+ channels in the plasma membrane of activated mast cells is a localized event and that Ca2+ acts locally within the cell to initiate exocytosis.

show abstract

Section: Discussionsupporting

confidence: 68%

Localized mast cell degranulation induced by concanavalin A-sepharose beads. Implications for the Ca2+ hypothesis of stimulus-secretion coupling.

Lawson¹,

Fewtrell²,

Raff³

1978

The Journal of Cell Biology

View full text Add to dashboard Cite

show abstract

“…The nature of this receptor is presently unknown, and the fact that Con A can induce histamine release raised the hypothesis that Con A was interacting with this receptor. This premise was weak ened by the recent report [6] which showed that Con-A-induced histam ine release in human basophils can be inhibited by monomer-Fc-specific anti-IgE; this finding indicated that Con A activation of basophils is most likely mediated by the sugar moieties on the Fc portion of the membrane-bound IgE.…”

Section: Introductionmentioning

confidence: 77%

<i>In vitro</i> Studies of Concanavalin-A-Induced Histamine Release from Human Basophils: Excess Bridging in the Inhibitory Region of the Dose-Response Curve

Magro¹

1974

Int Arch Allergy Immunol

Self Cite

View full text Add to dashboard Cite

Concanavalin-A (Con A)-induced histamine release from human basophils was studied in vitro. The quantity of histamine released was accurately measured by a spectrofluorometric assay. It was determined that release induced by lower doses of Con A (suboptimum) is inhibited by monomer-Fc-specific anti-IgE whereas release induced by high doses of Con A (supraoptimum) is enhanced by the monomer: In addition, release induced by a near optimum concentration of antigen E can be inhibited by increasing concentrations of Con A. The data indicate that high concentrations of Con A render the basophil unresponsive by excess bridging and it appears that this cell turn-off is mediated by the membrane-bound IgE.

show abstract

“…(Histamine release curves are plots of the fraction of a cell's total histamine that is released in a given time versus the logarithm of the concentration of ligand the cell is exposed to.) In addition, for ligand concentrations where receptor aggregate formation is high and histamine release low, the addition of monovalent hapten, which reduces the number of receptors in dimers, increases histamine release (Magro & Alexander, 1974;Magro & Bennich, 1977). In model simulations, the same manipulation increases Syk activation (Figure 4).…”

Section: Discussionmentioning

confidence: 98%

“…A way to distinguish between Type I and Type II inhibition is by comparing responses to anti-IgE in the presence and absence of Fab fragments (Magro & Alexander, 1974;Magro & Bennich, 1977). Adding monovalent ligand that competes for the same binding site as a multivalent ligand will always reduce the number of cross-links.…”

Section: Effect Of Monovalent Ligands On Syk Activationmentioning

confidence: 99%

Mathematical Modeling of Syk Activation in Allergen-Stimulated Mast Cells and Basophils

Nag¹,

Monine²,

Goldstein³

et al. 2012

Advances in Protein Kinases

View full text Add to dashboard Cite

Involvement of IgE in con A-induced histamine release from human basophils in vitro

Cited by 39 publications

References 19 publications

Localized mast cell degranulation induced by concanavalin A-sepharose beads. Implications for the Ca2+ hypothesis of stimulus-secretion coupling.

Localized mast cell degranulation induced by concanavalin A-sepharose beads. Implications for the Ca2+ hypothesis of stimulus-secretion coupling.

<i>In vitro</i> Studies of Concanavalin-A-Induced Histamine Release from Human Basophils: Excess Bridging in the Inhibitory Region of the Dose-Response Curve

Mathematical Modeling of Syk Activation in Allergen-Stimulated Mast Cells and Basophils

Contact Info

Product

Resources

About