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International Immunology Advance Access originally published online on June 23, 2005
International Immunology 2005 17(7):951-957; doi:10.1093/intimm/dxh276
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© The Japanese Society for Immunology. 2005. All rights reserved. For permissions, please e-mail: journals.permissions@oupjournals.org

Autistic effector T cells in mice with a point mutation in the LAT adaptor fail to respond to Listeria monocytogenes infection

Immo Prinz1,2, Mischo Kursar1,2, Hans-Willi Mittrücker2, Enrique Aguado2,3, Ulrich Steinhoff2, Stefan H. E. Kaufmann2 and Bernard Malissen1

1 Centre d'Immunologie de Marseille-Luminy, INSERM-CNRS-Université de la Méditerranée, Parc Scientifique de Luminy, Case 906, 13288 Marseille Cédex 9, France
2 Max Planck Institute for Infection Biology, Department of Immunology, Schumannstraße 21-22, D-10117 Berlin, Germany
3 Departamento de Bioquímica B e Inmunología, Facultad de Medicina, Universidad de Murcia, 30100 Murcia, Spain

Correspondence to: I. Prinz; E-mail: prinz{at}ciml.univ-mrs.fr

The adaptor protein linker for activation of T cells (LAT) is an important transducer of extracellular T cell stimuli. In mice with a point mutation in LAT (LatY136F), TCR signaling is substantially compromised and LatY136F T cells are unresponsive to CD3 cross-linking in vitro. Nevertheless, LatY136F mice develop a polyclonal lymphoproliferation of CD4+ T cells, which display a Th2-polarized effector phenotype. In this study, LatY136F mice were infected with the intracellular bacterium Listeria monocytogenes and the antigen-specific responses of T cells were determined. Both CD4+ and CD8+ LatY136F T cells were unresponsive to L. monocytogenes infection. In contrast, when CD4+ T cells from wild-type mice were adoptively transferred into LatY136F hosts, they responded normally to L. monocytogenes, indicating that the LatY136F milieu permits Th1 responses. Furthermore, we analyzed whether the infection would influence the capacity of LatY136F CD4+ T cells to produce IL-4 and IFN-{gamma}. While L. monocytogenes infection results in Th1-type T cell responses in wild-type animals, we found that it did not shift the strong Th2 polarization of LatY136F T cells towards a Th1 pattern. In conclusion, our results suggest that the activation and Th2 polarization of the LatY136F CD4+ T cells is not influenced by infection with an intracellular pathogen known to induce robust Th1 responses, and is thus likely driven by T cell intrinsic mechanisms.

Keywords: LatY136F mutation, linker for activation of T cells (LAT), Listeria monocytogenes, signal transduction, T cell activation, Th1/Th2 cells

Transmitting editor: T. Hünig


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