Journal of Leukocyte Biology Myeloid cells, immune suppression, tumor immunology
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Originally published online as doi:10.1189/jlb.0207108 on August 16, 2007

Published online before print August 16, 2007
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(Journal of Leukocyte Biology. 2007;82:1166-1173.)
© 2007 by Society for Leukocyte Biology

Stimulatory and costimulatory effects of IL-18 directed to different small intestinal CD43 T cell subsets

Dina Montufar-Solis, Heuy-Ching Wang and John R. Klein1

Department of Diagnostic Sciences, University of Texas Health Science Center at Houston, Dental Branch, Houston, Texas, USA

1 Correspondence to: University of Texas Health Science Center at Houston Department of Diagnostic Sciences Dental Branch 6516 MD Anderson Blvd. Houston, TX 77030, USA. E-mail: john.r.klein{at}uth.tmc.edu

This study has examined the stimulatory and costimulatory effects of IL-18 on two subsets of murine small intestinal intraepithelial lymphocytes (IELs) defined by the expression of the CD43 S7 glycoform. Data from gene array studies and real-time PCR indicated that S7+ IELs had significantly higher levels of gene expression for the IL-18 receptor and the IL-18R accessory protein than S7– IELs. IL-18 costimulation of IELs in conjunction with CD3-induced activation resulted in significantly greater proliferation than CD3 stimulation alone. In CFSE dilution experiments, IL-18 costimulation favored the S7+ IEL population. IL-18 costimulation did not affect apoptosis of either S7– or S7+ IELs compared with CD3 stimulation alone. Although IL-18 costimulation did not alter the total number of IFN-{gamma}-producing cells relative to CD3 stimulation alone, twice as many S7+ IELs were IFN-{gamma} -secreting cells than S7– IELs in both CD3-stimulated and IL-18-costimulated cultures. Notably, direct IL-18 stimulation in the absence of CD3 activation induced an IFN-{gamma} response that was predominantly directed to the S7+ population, indicating that IL-18 is itself an IFN-{gamma} activational signal for intestinal T cells. In contrast, direct IL-18 stimulation of IELs did not generate TNF-{alpha}-producing cells, indicating a differential response in the activation of proinflammatory cytokines following IL-18 exposure. These findings point to distinctly different activational effects of IL-18 on IELs, both with regard to the type of functional responses elicited and with respect to the IEL subsets affected.

Key Words: costimulation • cytokine • mucosa • T cells






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