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-Producing CD4+ T Cells Depend on Tissue Origin and Microbial Stimulus1
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* Experimental Rheumatology, Medical Clinic, Charité University Medicine Berlin, Berlin, Germany;
German Rheumatism Research Center (DRFZ), Berlin, Germany;
Department of Pathology, Stanford University School of Medicine, Stanford University, Stanford, CA 94305;
Center for Molecular Biology and Medicine, Veterans Affairs Palo Alto Health Care System, Palo Alto, CA 94304;
¶ Department of Pediatrics and the Immunology Program, Stanford University School of Medicine, Stanford, CA;
|| Benaroya Research Institute at Virginia Mason, Seattle, WA 98101;
# Department of Immunology, University of Washington School of Medicine, Seattle, WA 98195;
** Center for Infectious Diseases, University of Würzburg, Germany; and
Department of Immunology, Friedrich-Schiller Universität, Medical School, Jena, Germany
Th1- and Th2-polarized immune responses are crucial in the defense against pathogens but can also promote autoimmunity and allergy. The chemokine receptors CXCR3 and CCR4 have been implicated in differential trafficking of IFN-
- and IL-4-producing T cells, respectively, but also in tissue and inflammation-specific homing independent of cytokine responses. Here, we tested whether CD4+ T cells isolated from murine tissues under homeostatic or inflammatory conditions exhibit restricted patterns of chemotactic responses that correlate with their production of IFN-, IL-4, or IL-10. In uninfected mice, IL-4-producing T cells preferentially migrated to the CCR4 ligand, CCL17, whereas IFN--expressing T cells as well as populations of IL-4+ or IL-10+ T cells migrated to the CXCR3 ligand, CXCL9. All cytokine-producing T cell subsets strongly migrated to the CXCR4 ligand, CXCL12. We assessed chemotaxis of T cells isolated from mice infected with influenza A virus or the nematode Nippostrongylus brasiliensis, which induce a strong Th1 or Th2 response in the lung, respectively. Unexpectedly, the chemotactic responses of IL-4+ T cells and T cells expressing the immunosuppressive cytokine IL-10 were influenced not only by the strongly Th1- or Th2-polarized environments but also by their anatomical localization, i.e., lung or spleen. In contrast, IFN-+ T cells exhibited robust chemotaxis toward CXCL9 and had the most consistent migration pattern in both infection models. The results support a model in which the trafficking responses of many effector and regulatory T cells are regulated as a function of the infectious and tissue environments.
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