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*
Graduate Program in Immunology and
Department of Ophthalmology, University of Texas Southwestern Medical Center, Dallas, TX 75235
Ocular immune privilege is the result of several unique features of
the eye, including the systemic down-regulation of Th1 immune responses
to Ags encountered in the anterior chamber of the eye—a phenomenon
termed anterior chamber-associated immune deviation (ACAID). The
induction of ACAID requires the participation of three cell
populations: the ocular ACAID APC, the splenic B cell, and the splenic
T cell. Because B cells have been implicated in tolerogenic Ag
presentation in other systems, we hypothesized that B cells were
responsible for the induction of regulatory T cells in ACAID. The
central hypothesis for this study is that APC from the eye migrate to
the spleen where they release antigenic peptides (OVA) that are
captured and presented to T cells by splenic B cells. A combination of
in vitro and in vivo studies demonstrated that splenic B cells,
incubated with ACAID APC in vitro, were capable of inducing ACAID when
transferred to naive mice. The induction of ACAID required the normal
expression of 
2-microglobulin on both the B cell and
ACAID APC, but not on the T suppressor cells. Moreover, the induction
of ACAID regulatory cells required histocompatibility between the B
cells and regulatory T cells at the TL/Qa region. The results indicate
that: 1) B cells are necessary for the induction of ACAID; 2) ACAID B
cells do not directly suppress the expression of delayed-type
hypersensitivity; and 3) the induction of Ag-specific regulatory T
cells by ACAID B cells requires histocompatibility at the TL/Qa
region.
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