P- and E-selectin mediate recruitment of T-helper-1 but not T-helper-2 cells into inflamed tissues

Frank Austrup, Dietmar Vestweber, Eric Borges, Max Löhning, Rolf Bräuer, Udo Herz, Harald Renz, Rupert Hallmann, Alexander Scheffold, Andreas Radbruch and Alf Hamann
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Frank Austrup: Universitätskrankenhaus Eppendorf
Dietmar Vestweber: Universität Münster
Eric Borges: Universität Köln
Max Löhning: Universität Köln
Rolf Bräuer: Klinikum des Friedrich-Schiller-Universität
Udo Herz: Virchow-Klinikum des Humboldt Universität
Harald Renz: Virchow-Klinikum des Humboldt Universität
Rupert Hallmann: Universität Erlangen-Nürnberg
Alexander Scheffold: Universität Köln
Andreas Radbruch: Universität Köln
Alf Hamann: Universitätskrankenhaus Eppendorf

Nature, 1997, vol. 385, issue 6611, 81-83

Abstract: Abstract WHEN activated, T helper cells differentiate into one of two subsets, Th1 and Th2, characterized by distinct profiles of cytokine production. Th1 cells activate pro-inflammatory effector mechanisms involved in protection and autoimmunity, whereas Th2 cells induce humoral and allergic responses and downregu-late local inflammation1,2. Apart from differences in the repertoire of cytokines, no phenotypic attributes are established that distinguish the two subsets. Here we show that Th1 cells, but not Th2 cells, are able to bind to P-selectin and E-selectin. Moreover, only Th1 cells can efficiently enter inflamed sites in Th1-dominated models, such as sensitized skin or arthritic joints, but not in a Th2-dominated allergic response. Immigration of Th1 cells into inflamed skin can be blocked by antibodies against P- and E-selectin. These results provide evidence for adhesion mechanisms to distinguish between the two T helper subsets and mediate their differential trafficking. They indicate that selective recruitment is an additional level of regulation for both effector function profile and character of a local immune response.

Date: 1997
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DOI: 10.1038/385081a0

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