Reversible binding of multivalent antigen in the control of B lymphocyte activation

Gandolfi, Alberto; Giovenco, Maria Adelaide; Strom, Roberto

doi:10.1016/0022-5193(78)90238-2

Cited by 11 publications

(5 citation statements)

References 22 publications

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“…The fraction of receptors in aggregates of all sizes, which has been proposed as a measure of the extent of receptor cross-linking (Gandolfi et al, 1978;Perelson, 1981), is given by ␣(2). Receptor aggregates of size 10 or more, termed immunons, have been suggested to be the minimum signaling unit for B cells (Dintzis et al, 1976(Dintzis et al, , 1983.…”

Section: Quantifying Receptor Aggregationmentioning

confidence: 99%

“…The theory for these ligands has been refined over a number of years (Posner et al, 1995b) and applied to a number of problems, particularly the analysis of Fc⑀RI aggregation on the surface of rat basophilic leukemia cells (Goldstein, 1988;Goldstein and Wofsy, 1994). Theoretical work on multivalent ligands (Gandolfi et al, 1978;DeLisi, 1980;Perelson, 1981) has also been applied to a number of problems in immunology and virology (Hlavacek et al, 1999;Sulzer and Perelson, 1997;Dee and Shuler, 1997;Goldstein and Wofsy, 1996;Wickham et al, 1990Wickham et al, , 1995Segal et al, 1983;Vogelstein et al, 1982;. However, models for multivalent ligands have yet to be fully developed.…”

Section: Introductionmentioning

confidence: 99%

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Steric Effects on Multivalent Ligand-Receptor Binding: Exclusion of Ligand Sites by Bound Cell Surface Receptors

Hlavacek

Posner

Perelson

1999

Biophysical Journal

135

133

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Steric effects can influence the binding of a cell surface receptor to a multivalent ligand. To account for steric effects arising from the size of a receptor and from the spacing of binding sites on a ligand, we extend a standard mathematical model for ligand-receptor interactions by introducing a steric hindrance factor. This factor gives the fraction of unbound ligand sites that are accessible to receptors, and thus available for binding, as a function of ligand site occupancy. We derive expressions for the steric hindrance factor for various cases in which the receptor covers a compact region on the ligand surface and the ligand expresses sites that are distributed regularly or randomly in one or two dimensions. These expressions are relevant for ligands such as linear polymers, proteins, and viruses. We also present numerical algorithms that can be used to calculate steric hindrance factors for other cases. These theoretical results allow us to quantify the effects of steric hindrance on ligand-receptor kinetics and equilibria.

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Section: Quantifying Receptor Aggregationmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Steric Effects on Multivalent Ligand-Receptor Binding: Exclusion of Ligand Sites by Bound Cell Surface Receptors

Hlavacek

Posner

Perelson

1999

Biophysical Journal

135

133

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“…Modeling this mode follows the formalisms previously developed (Gandolfi, 1978;Perelson, 1981) that were used to analyze the attachment of multivalent ligands. Only a minor modification is made to include a binding state that accounts for the nonspecific binding that nearly all viruses exhibit, particularly those such as Vesicular Stomatitis virus and closely related viruses (Schlegel et al, 1982).…”

Section: Modementioning

confidence: 99%

“…The multivalent attachment of antigens where receptors are explicitly taken into account has been previously modeled (Macken and Perelson, 1982;Perelson, 1981;DeLisi, 1980b;Perelson and DeLisi, 1980;Gandolfi et al, 1978). However, because significant differences exist between viruses and multivalent antigens, an extension of this work is necessary to apply it to viral binding.…”

Section: Introductionmentioning

confidence: 99%

General analysis of receptor-mediated viral attachment to cell surfaces

Wickham

Granados

Wood

et al. 1990

Biophysical Journal

101

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Viruses are multivalent particles that attach to cells through one or more bonds between viral attachment proteins (VAP) and specific cellular receptors. Three modes of virus binding are presented that can explain the diversity in binding data observed among viruses. They are based on multivalency of attachment and spatial versus receptor saturation effects which are easily distinguished based upon simple criteria. Mode 1 involves only monovalent virus/receptor binding. Modes 2 and 3 involve multivalent bonds between the virus and cell; however, in mode 3 space on the cell surface becomes saturated before receptors. A model is developed for viral attachment that accounts for nonspecific binding, receptor/virus interactions, and spatial saturation effects. The model can describe each mode in different limits and can be applied to virus binding data to extract key physical information such as receptor number and affinity. These values are used to postulate the type of VAP/receptor interaction involved and to predict binding at different parameter values. For the mode 2 binding of Adenovirus 2, the model predicts a receptor number of 4-15 x 10(3) on HeLa cells and an affinity of 2-6 x 10(7) M-1 which closely approximate experimental estimates. For the binding of three, broad-host-range, enveloped viruses, Semliki Forest virus, Vesicular Stomatitis virus, and the baculovirus, Autographa californica nuclear polyhedrosis virus, the model predicts receptor numbers of 10(5) or greater and affinities in the range of 10(4) to 10(5) M-1. These values are indicative of a VAP/oligosaccharide interaction which has been documented for a number of other viruses. Experimental evidence is presented that is the first to demonstrate that baculovirus binding is mediated by a cell surface receptor.

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“…Equations 10A-G also follow as a special case of previously developed theories (Gondolfi et al, 1978;DeLisi, 1980;Perelson, 1981).…”

Section: Ron¡=imentioning

confidence: 99%

Mechanism of binding of multivalent immune complexes to Fc receptors. 1. Equilibrium binding

Dower¹,

DeLisi²,

Titus³

et al. 1981

Biochemistry

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Reversible binding of multivalent antigen in the control of B lymphocyte activation

Cited by 11 publications

References 22 publications

Steric Effects on Multivalent Ligand-Receptor Binding: Exclusion of Ligand Sites by Bound Cell Surface Receptors

Steric Effects on Multivalent Ligand-Receptor Binding: Exclusion of Ligand Sites by Bound Cell Surface Receptors

General analysis of receptor-mediated viral attachment to cell surfaces

Mechanism of binding of multivalent immune complexes to Fc receptors. 1. Equilibrium binding

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