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(Journal of Leukocyte Biology. 2002;72:780-789.)
© 2002 by Society for Leukocyte Biology

Role of the autocrine chemokines MIP-1 and MIP-1ß in the metastatic behavior of murine T cell lymphoma

Patricia Menten^*, Alessandra Saccani^*, Chris Dillen^*, Anja Wuyts^*, Sofie Struyf^*, Paul Proost^*, Alberto Mantovani, Ji Ming Wang and Jo Van Damme^*

^* Laboratory of Molecular Immunology, Rega Institute for Medical Research, Leuven, Belgium;
Istituto di Ricerche Farmacologiche Mario Negri, Milan, Italy; and
National Cancer Institute, National Institutes of Health, Frederick, Maryland

Correspondence: Dr. J. Van Damme, Laboratory of Molecular Immunology, Rega Institute for Medical Research, Minderbroedersstraat 10, B-3000 Leuven, Belgium. E-mail: jozef.vandamme{at}rega.kuleuven.ac.be

The ESb-MP T-cell line is a highly malignant murine lymphoma, which preferentially metastasizes toward the kidney. This could be a result of the local production of monocyte chemoattractant protein-1 (MCP-1) and regulated on activation, normal T expressed and secreted (RANTES), which are chemotactic for ESb-MP cells. Here, we demonstrate that ESb-MP cells are already responsive to the chemotactic activity of macrophage inflammatory protein-1 (MIP-1) and MIP-1ß from 1 ng/ml onward. Moreover, upon stimulation with lipopolysaccharide (LPS) or virus, ESb-MP cells themselves produce significant amounts of MIP-1 (200 ng/ml). Indeed, the major autocrine chemoattractants, isolated from ESb-MP cells, were intact MIP-1 and MIP-1ß. Pretreatment with LPS or addition of MIP-1 inhibited the in vitro migration of ESb-MP cells toward various chemokines. Moreover, compared with untreated lymphoma cells, LPS-treated cells produced significantly less metastasis in mice. The results represented here suggest that the role of chemokines in attracting tumor cells at secondary sites depends on a balance between autocrine-produced and tissue-derived chemokines. This delicate balance should be considered in the design of antichemokine strategies in different tumor types.

Key Words: migration • metastasis • endotoxin

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