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The Type 1 Cysteinyl Leukotriene Receptor Triggers Calcium Influx and Chemotaxis in Mouse - and Effector T Cells¹

Immo Prinz^*, Claude Gregoire^*, Hans Mollenkopf, Enrique Aguado^2,*, Ying Wang^*, Marie Malissen^*, Stefan H.E. Kaufmann and Bernard Malissen^3,*

^* Centre d’Immunologie de Marseille-Luminy, Institut National de la Santé et de la Recherche Médicale-Centre National de la Recherche Scientifique-Université de la Méditerranée, Parc Scientifique de Luminy, Marseille, France; and Microarray Core Facility, and Department of Immunology, Max Planck Institute for Infection Biology, Berlin, Germany

Linker for activation of T cells (LAT) is essential for T cell activation. Mice with mutations of distinct LAT tyrosine residues (LatY136F and Lat3YF) develop lymphoproliferative disorders involving TCR or T cells that trigger symptoms resembling allergic inflammation. We analyzed whether these T cells share a pattern of gene expression that may account for their pathogenic properties. Both LatY136F and Lat3YF T cells expressed high levels of the type 1 cysteinyl leukotriene receptor (CysLT₁). Upon binding to the 5(S)-hydroxy-6(R)-S-cysteinylglycyl-7,9-trans-11,14-cis-eicosatetraenoic acid (LTD₄) cysteinyl leukotriene, CysLT₁ induced Ca²⁺ flux and caused chemotaxis in both LatY136F and Lat3YF T cells. Wild-type in vitro-activated T cells, but not resting T cells, also migrated toward LTD₄ however with a lower magnitude than T cells freshly isolated from LatY136F and Lat3YF mice. These results suggest that CysLT₁ is likely involved in the recruitment of activated and T cells to inflamed tissues.

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