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CD4⁺ T Cell Polarization in Mice Is Modulated by Strain-specific Major Histocompatibility Complex–independent Differences within Dendritic Cells

Christophe Filippi, Stéphanie Hugues, Julie Cazareth, Valérie Julia, Nicolas Glaichenhaus and Sophie Ugolini

E03-44, Institut National de la Santé et de la Recherche Médicale, University of Nice-Sophia Antipolis, 06560 Valbonne, France

Address correspondence to N. Glaichenhaus, E03-44, Institut National de la Santé et de la Recherche Médicale, University of Nice-Sophia Antipolis, 660 Route des Lucioles, 06560 Valbonne, France. Phone: 33-4-93-95-77-85; Fax: 33-4-93-95-77-08; E-mail: glaichenhaus{at}ipmc.cnrs.fr; or S. Ugolini at his present address Centre d'Immunologie de Marseille-Luminy, Case 906 Parc Scientifique de Luminy, 13288 Marseille Cedex 09, France. Phone: 33-4-91-26-94-32; Fax: 33-4-91-26-94-30; E-mail: ugolini{at}ciml.univ-mrs.fr

Resistance and susceptibility to Leishmania major in mice are determined by multiple genes and correlate with the preferential development of Th1 and Th2 responses, respectively. Here, we found that CD11b⁺ dendritic cells (DCs) prime parasite-specific CD4⁺ T cells in both susceptible BALB/c (H2-d) and resistant B10.D2 (H2-d) mice. However, BALB/c and B10.D2 DCs from L. major–infected mice differ in their ability to polarize naive T cells into Th1 or Th2 effector cells. This difference is cell-intrinsic, is not restricted to H2-d mice, and is observed with both parasite-specific and allospecific CD4⁺ T cells. Thus, strain-specific differences within CD11b⁺ DCs influence the ability of inbred mice to mount polarized CD4⁺ T cell responses.

Key Words: Ag presentation • T cell differentiation • intracellular pathogen • cytokine secretion • Leishmania major

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