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Originally published online as doi:10.1189/jlb.0705414 on January 13, 2006

Published online before print January 13, 2006
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(Journal of Leukocyte Biology. 2006;79:676-685.)
© 2006 by Society for Leukocyte Biology

Characterizing the circulating, gliadin-specific CD4+ memory T cells in patients with celiac disease: linkage between memory function, gut homing and Th1 polarization

Shomron Ben-Horin*,1, Peter H. R. Green{dagger}, Ilan Bank{ddagger}, Leonard Chess* and Itamar Goldstein*,2

* Department of Medicine and
{dagger} Celiac Disease Center, College of Physicians and Surgeons of Columbia University, New York, New York; and
{ddagger} Department of Medicine, Chaim Sheba Medical Center and Tel Aviv University, Tel Hashomer, Israel

2Correspondence: The Sheba Cancer Research Center, Chaim Sheba Medical Center, Tel Hashomer 52621, Israel. E-mail: itamar.goldstein{at}sheba.health.gov.il

ABSTRACT

Celiac disease (CD) is a chronic, immune-mediated disorder of the gut, driven by T cells reacting locally to a distinct antigen, gliadin. Thus, CD offers the opportunity to study the T cell memory response to gliadin and whether gut tropism and T helper cell type 1 (Th1) polarization, which characterize the effector phase, are preserved in the memory progeny. It is notable that previous studies yielded conflicting results as to the presence of gliadin-specific memory CD4+ T cells in the peripheral blood of CD patients. However, we used a different and highly sensitive approach based on fluorescein-derived label dilution, whereby the memory cells are identified operationally by their greater capacity to proliferate upon re-encounter with antigen. Thus, using flow cytometry, we could resolve multiple successive generations as well as immunophenotype the dividing cells. Here, we show that the peripheral blood lymphocyte of some CD patients on a gliadin-free diet, but not healthy donors, contains a detectable population of CD4+ memory T cells specific for deamidated gliadin. Moreover, these gliadin-specific memory T cells are marked by a distinctive phenotype: They express high levels of the gut-homing ß7 integrins and primarily produce interferon-{gamma} and tumor necrosis factor {alpha}. We conclude that memory for gliadin-derived antigens within the circulating CD4+ T cells is linked with gut tropism as well as Th1 polarization.

Key Words: human • cell trafficking • adhesion molecules




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