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J. Biol. Chem., Vol. 279, Issue 7, 5641-5647, February 13, 2004

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Ca²⁺ Signaling in Identified T-lymphocytes from Human Intestinal Mucosa

RELATION TO HYPOREACTIVITY, PROLIFERATION, AND INFLAMMATORY BOWEL DISEASE^*

Alexander Schwarz, Eberhard Tutsch, Bianca Ludwig, Eva C. Schwarz, Andreas Stallmach, and Markus Hoth¶

From the Departments of Physiologie and Internal Medicine II, University of the Saarland, D-66421 Homburg, Germany

Ca²⁺ entry across the plasma membrane is necessary for the activation and proliferation of T-lymphocytes. Human intestinal lamina propria lymphocytes physiologically exhibit minimal proliferation in response to antigen receptor stimulation when compared with peripheral blood T-lymphocytes. This hyporeactivity is partially abolished in inflammatory bowel disease. We hypothesized that differences in Ca²⁺ signaling could be related to the disease. To test this possibility, we measured Ca²⁺ signals in identified lymphocytes from human blood and human intestinal mucosa. Ca²⁺ signals in lamina propria T-lymphocytes from non-inflamed tissue were drastically reduced when compared with Ca²⁺ signals of blood T-lymphocytes from the same persons. However, Ca²⁺ signals in T-lymphocytes from inflamed intestinal mucosa were much higher than the ones from non-inflamed mucosa and almost reached levels of Ca²⁺ signals in peripheral blood T-cells. Furthermore, Ca²⁺ influx was closely linked to cell proliferation in both peripheral blood T-lymphocytes and lamina propria lymphocytes cells. We conclude that differences in Ca²⁺ signaling can explain the differences of T-lymphocyte reactivity in blood versus lamina propria and, importantly, also between T-lymphocytes from inflamed and non-inflamed intestinal mucosa. Ca²⁺ channels in the plasma membrane of T-lymphocytes might thus prove an excellent target to screen for immunosuppressiva to potentially treat the symptoms of inflammatory bowel disease.

Received for publication, August 22, 2003 , and in revised form, October 14, 2003.

^* This work was in part supported by the Sonderforschungsbereich 530 (Teilprojekt A3) (to M. H.), Deutsche Forschungsgemeinschaft Grant HO 2190/1-1 (to M. H. and A. Stallmach), the Graduiertenkolleg "Cellular Regulation and Proliferation" (to A. Stallmach and M. H.), and a research fellowship from the Deutsche Morbus Crohn/Colitis ulcerosa Vereinigung (DCCV-e.V.) (to A. Schwarz). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

^¶ To whom correspondence should be addressed: Institut für Physiologie, Gebäude 58, Universität des Saarlandes, D-66421 Homburg/Saar, Germany. Tel.: 49-6841-1626266; Fax: 49-6841-1626060; E-mail: markus.hoth{at}uniklinik-saarland.de.

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