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,*
*
University of Alabama, Birmingham, AL 35294; and
Hospital for Children and Adolescents, University of Helsinki, Helsinki, Finland
Animal experiments show that lymphocytes activated in the intestine
circulate through mesenteric lymph nodes, lymphatics, and blood,
returning to the gut. Homing into intestinal lamina propria is mediated
by lymphocyte surface homing receptors, mainly the
4ß7-integrin. We studied in humans whether
intestinal T cells entering the blood upon antigenic activation would
exhibit homing commitments to the gut. Volunteers were immunized with
keyhole limpet hemocyanin (KLH) first orally and then parenterally or
only parenterally, and the expression of
4ß7 on T cells specific for KLH or tetanus
toxoid was studied. Circulating T cells were depleted of
4ß7+ cells by immunomagnetic
selection. This depletion removed a significant proportion of the
KLH-specific cells (mean decrease in proliferative response of 71%) in
the orally immunized volunteers. No difference in the KLH-induced
proliferation was found between the total and the
4ß7-depleted populations in volunteers
parenterally immunized with KLH, regardless of whether a preceding
mucosal priming had taken place or not. In both immunization groups,
the depletion of 4ß7+ cells
had no influence on the proliferative response to tetanus toxoid. We
conclude that, in contrast to T cells activated by parenteral
immunization, gut-derived T cells have preferential homing commitments
to the gut. This commitment was no longer observed after a subsequent
parenteral Ag administration. Besides showing that the site of Ag
encounter determines the expression of homing receptors, the present
study is the first to provide evidence for a circulation of newly
activated Ag-specific intestinal T cells back to the gut in
humans.
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