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,
Immunobiology Vaccine Center, Departments of
*
Oral Biology and
Microbiology, University of Alabama Medical Center, Birmingham, AL 35294; and
Department of Mucosal Immunology, Research Institute for Microbial Diseases, Osaka University, Suita, Osaka, Japan
Epithelial cells and lymphocytes, including 
and 
ß T
cells, in the gastrointestinal tract epithelium represent a major host
defense intranet that is incompletely understood. Cell-to-cell
interactions between intraepithelial lymphocytes (IELs) and intestinal
epithelial cells (IECs) comprise this intranet, and we have assessed
the role of IECs in the regulation of and ß T cell
responses. When highly purified CD3+ IEL T cells were
stimulated via the TCR-CD3 complex, high proliferative responses and
cytokine synthesis were induced. However, the addition of viable IECs
or purified IEC membranes (mIEC) down-regulated T cell proliferative
and cytokine responses. Further, the inhibitory effect of mIEC was not
restored by antibodies to TGF-ß, CD1d, E-cadherin, or MHC class I or
II. This inhibitory effect was noted for both and ß T cell
subsets from IELs, and mRNA levels were reduced for both Th1 (IL-2 and
IFN-) and Th2 (IL-4 and IL-5) cytokines in and ß IELs.
In contrast, a purified membrane fraction obtained from thymocytes did
not inhibit IEL proliferative responses. Further, mIEC did not inhibit
splenic ß T cell proliferative responses. These findings show that
cell-to-cell interactions between intraepithelial and ß T
cells and IECs occur via cell surface molecules, suggesting an intranet
to prevent potential inflammatory responses at the intestinal mucosal
surface.
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