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Infection and Immunity, November 2003, p. 6178-6183, Vol. 71, No. 11
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.11.6178-6183.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Differential Production of Macrophage Inflammatory Protein 1 (MIP-1), Lymphotactin, and MIP-2 by CD4⁺ Th Subsets Polarized In Vitro and In Vivo

Kerstin Müller,^1, Susanne Bischof,² Frank Sommer,² Michael Lohoff,² Werner Solbach,¹ and Tamás Laskay^2*

Institute for Medical Microbiology and Hygiene, University of Lübeck, Lübeck,¹ Institute for Medical Microbiology and Hygiene, University of Marburg, Marburg, Germany²

Received 23 December 2002/ Returned for modification 21 March 2003/ Accepted 6 August 2003

Due to differential expression of chemokine receptors, the Th1 and Th2 subsets of CD4⁺ T cells differ in their migratory responses to chemokines. These differences in the migration patterns are likely to play a role in the initiation and regulation of Th1 and Th2 immune responses, inflammatory processes, and T-cell-mediated pathology. In the present study we evaluated the role of activated Th cells as producers of chemokines. Three different sources of murine Th cells were used, i.e., long-term-cultured Th1 and Th2 cell clones, Th1 and Th2 cells differentiated from naïve CD4⁺ spleen and lymph node cells in vitro, and Th1 and Th2 subsets polarized in vivo using a murine experimental Leishmania major infection model. Following stimulation with anti-CD3, macrophage inflammatory protein 1 (MIP-1) and lymphotactin were produced selectively by Th1 cells but not by Th2 cells. In contrast, only Th2 cells produced MIP-2. The possible biological relevance of these data was substantiated by the finding that in vivo-polarized Th1 cells, but not Th2 cells, produced MIP-1 and lymphotactin while in vivo-polarized Th2 cells secreted MIP-2. The above data demonstrate that Th1 and Th2 cells differ in their ability to produce chemokines, suggesting that Th1 and Th2 subsets differentially contribute to recruitment of cells into inflammatory foci.

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* Corresponding author. Mailing address: Institute for Medical Microbiology and Hygiene, University of Lübeck, Ratzeburger Allee 160, D-23538 Lübeck, Germany. Phone: 49-451-500-2797. Fax: 49-451-500-2808. E-mail: Tamas.Laskay{at}hygiene.ukl.mu-luebeck.de.

Editor: J. M. Mansfield

Present address: Institute of Radiobiology, German Armed Forces, D-80937 Munich, Germany.

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Infection and Immunity, November 2003, p. 6178-6183, Vol. 71, No. 11
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.11.6178-6183.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

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