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Biophys J, February 2001, p. 606-612, Vol. 80, No. 2
and
*Department of Mathematics and Statistics, University of New
Mexico, Albuquerque, New Mexico 87131; Program in Applied
Mathematics, University of Arizona, Tucson, Arizona 85721; and
Theoretical Biology and Biophysics Group, Theoretical
Division, Los Alamos National Laboratory, Los Alamos, New Mexico
87545 USA
The serial engagement model provides an attractive and
plausible explanation for how a typical antigen presenting cell,
exhibiting a low density of peptides recognized by a T cell, can
initiate T cell responses. If a single peptide displayed by a major
histocompatibility complex (MHC) can bind, sequentially, to different T
cell receptors (TCR), then a few peptides can activate many receptors.
To date, arguments supporting and questioning the prevalence of serial engagement have centered on the down-regulation of TCR after contact of
T cells with antigen presenting cells. Recently, the existence of
serial engagement has been challenged by the demonstration that
engagement of TCR can down-regulate nonengaged bystander TCR. Here we
show that for binding and dissociation rates that characterize
interactions between T cell receptors and peptide-MHC, substantial
serial engagement occurs. The result is independent of mechanisms and
measurements of receptor down-regulation. The conclusion that single
peptide-MHC engage many TCR, before diffusing out of the contact region
between the antigen-presenting cell and the T cell, is based on a
general first passage time calculation for a particle alternating
between states in which different diffusion coefficients govern its transport.
Biophys J, February 2001, p. 606-612, Vol. 80, No. 2
© 2001 by the Biophysical Society 0006-3495/01/02/606/07 $2.00
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