Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2005-12-20
pubmed:abstractText
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-gamma- 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-gamma, IL-4, or IL-10. In uninfected mice, IL-4-producing T cells preferentially migrated to the CCR4 ligand, CCL17, whereas IFN-gamma-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-gamma+ 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.
pubmed:grant
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
176
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
557-66
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:16365450-Animals, pubmed-meshheading:16365450-CD4-Positive T-Lymphocytes, pubmed-meshheading:16365450-Chemokine CCL17, pubmed-meshheading:16365450-Chemokine CXCL9, pubmed-meshheading:16365450-Chemokines, CC, pubmed-meshheading:16365450-Chemokines, CXC, pubmed-meshheading:16365450-Chemotaxis, Leukocyte, pubmed-meshheading:16365450-Female, pubmed-meshheading:16365450-Flow Cytometry, pubmed-meshheading:16365450-Influenza A virus, pubmed-meshheading:16365450-Interferon-gamma, pubmed-meshheading:16365450-Interleukin-10, pubmed-meshheading:16365450-Interleukin-4, pubmed-meshheading:16365450-Lung, pubmed-meshheading:16365450-Male, pubmed-meshheading:16365450-Mice, pubmed-meshheading:16365450-Mice, Inbred BALB C, pubmed-meshheading:16365450-Nippostrongylus, pubmed-meshheading:16365450-Orthomyxoviridae Infections, pubmed-meshheading:16365450-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:16365450-Spleen, pubmed-meshheading:16365450-Strongylida Infections
pubmed:year
2006
pubmed:articleTitle
Chemotactic responses of IL-4-, IL-10-, and IFN-gamma-producing CD4+ T cells depend on tissue origin and microbial stimulus.
pubmed:affiliation
Experimental Rheumatology, Medical Clinic, Charité University Medicine Berlin, Berlin, Germany. debes@stanford.edu
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural