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International Immunology Advance Access published online on June 23, 2005
International Immunology, 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
Received January 11, 2005
Accepted April 27, 2005

Article

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

Immo Prinz 1*, Mischo Kursar 1, Hans-Willi Mittrücker 2, Enrique Aguado 3, Ulrich Steinhoff 2, Stefan H. E. Kaufmann 2, and Bernard Malissen 4

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

* To whom correspondence should be addressed.
Immo Prinz, E-mail: prinz{at}ciml.univ-mrs.fr


  Abstract

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.
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