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A Role for the Neuronal Protein Collapsin Response Mediator Protein 2 in T Lymphocyte Polarization and Migration¹

Peggy Vincent^*, Yves Collette, Romain Marignier^*, Carine Vuaillat^*, Véronique Rogemond^*, Nathalie Davoust^*, Christophe Malcus, Sylvie Cavagna^*, Antoine Gessain, Irma Machuca-Gayet^¶, Marie-Françoise Belin^*, Tam Quach^* and Pascale Giraudon^2,*

^* Institut National de la Santé et de la Recherche Médicale (INSERM) Unité 433 and Institut Fédératif de Recherche 19, Faculté de Médecine R. Laënnec, Lyon, France; INSERM Unité Mixte de Recherche (UMR) 599, Institut de Cancérologie de Marseille, Marseille, France; Laboratoire d’Immunologie-Hôpital Neurologique, Lyon, France; Unité d’Epidémiologie et Physiopathologie des virus oncogènes, Institut Pasteur, Paris, France; and ^¶ UMR 5161, Centre National de la Recherche Scientifique, Ecole Normale Supérieure de Lyon, Lyon, France

The semaphorin-signaling transducer collapsin response mediator protein 2 (CRMP2) has been identified in the nervous system where it mediates Sema3A-induced growth cone navigation. In the present study, we provide first evidence that CRMP2 is present in the immune system and plays a critical role in T lymphocyte function. CRMP2 redistribution at the uropod in polarized T cells, a structural support of lymphocyte motility, suggests that it may regulate T cell migration. This was evidenced in primary T cells by small-interfering RNA-mediated CRMP2 gene silencing and blocking Ab, as well as CRMP2 overexpression in Jurkat T cells tested in a chemokine- and semaphorin-mediated transmigration assay. Expression analysis in PBMC from healthy donors showed that CRMP2 is enhanced in cell subsets bearing the activation markers CD69⁺ and HLA-DR⁺. Heightened expression in T lymphocytes of patients suffering from neuroinflammatory disease with enhanced T cell-transmigrating activity points to a role for CRMP2 in pathogenesis. The elucidation of the signals and mechanisms that control this pathway will lead to a better understanding of T cell trafficking in physiological and pathological situations.

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