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Maximum Immunobioactivity of Murine Small Intestinal Intraepithelial Lymphocytes Resides in a Subpopulation of CD43⁺ T Cells¹

Heuy-Ching Wang^*, Dina Montufar-Solis^*, Ba-Bie Teng and John R. Klein^2,*

^* Department of Diagnostic Sciences, Dental Branch, and Research Center for Human Genetics, Institute of Molecular Medicine, University of Texas Health Science Center, Houston, TX 77030

CD43 has been linked to many function-associated T cell activities. Using mAbs that recognize two different CD43 determinants, we show that, although mouse small intestinal intraepithelial lymphocytes (IELs) expressed the CD43 core molecule reactive with mAb R2/60, only about one-half of the total IELs—including some but not all of the TCR and TCR cells—expressed the CD43 S7^– reactive determinant. CD43 S7⁺ IELs secreted more IL-2, IL-4, IL-10, IL-17, and IFN- following anti-CD3 stimulation, and were >4-fold more cytotoxic in fresh isolates and >16-fold more cytotoxic after anti-CD3 stimulation, than S7^– IELs. S7⁺ but not S7^– IELs from the ileum of IL-10^–/– mice spontaneously produced IFN-. In vivo BrdU uptake by IELs in non-Ag-primed mice was greatest in the S7⁺ population, indicating that significantly more S7⁺ IELs than S7^– IELs undergo cell expansion under normal homeostatic conditions. DNA microarray analyses showed that S7⁺ IELs expressed higher levels of genes associated with activated T cells, whereas S7^– IELs expressed genes used in the regulation of NK cells. These findings define two functionally distinct populations of IELs based on CD43 expression independent of TCR class, and they identify a subset of IELs that may serve as a target to better control intestinal inflammation.

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