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PMID: 21221121 Published · ppublish English Journal Article Research Support, N.I.H., Extramural Review

CXCR3 ligands: redundant, collaborative and antagonistic functions.

Immunology and cell biology ·Vol. 89 ·No. 2 ·2011-02-00 ·Pages 207-15

Groom JR, Luster AD

Abstract

CXCR3 is a chemokine receptor that is rapidly induced on naïve T cells following activation, and preferentially remains highly expressed on type-1 helper (Th1)-type CD4(+) T cells, effector CD8(+) T cells and innate-type lymphocytes, such as natural killer (NK) and NKT cells. CXCR3 is activated by three interferon (IFN)-γ-inducible ligands CXCL9 (monokine induced by gamma-interferon), CXCL10 (interferon-induced protein-10) and CXCL11 (interferon-inducible T-cell alpha chemoattractant). Although some studies have revealed that these ligands have redundant functions in vivo, other studies have demonstrated that the three CXCR3 ligands can also collaborate and even compete with each other. Differential regulation of the three ligands at specific times in defined anatomically restricted locations in vivo likely participates in the fine control of T-cell trafficking over the course of an immune response. Among the differences in regulation, CXCL10 is induced by a variety of innate stimuli that induce IFN-α/β as well as the adaptive immune cell cytokine IFN-γ, whereas CXCL9 induction is restricted to IFN-γ. In this review, we will discuss how the balance, timing and pattern of CXCR3 ligand expression appears to regulate the generation of effector T cells in the lymphoid compartment and subsequent migration into peripheral sites of Th1-type inflammation in which the CXCR3 ligands also then regulate the interactions and migratory behavior of effector T cells in an inflamed peripheral tissue.

MeSH Terms
Animals Humans Ligands Models, Immunological Receptors, CXCR3/antagonists & inhibitors,immunology
Chemicals
Ligands Receptors, CXCR3
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Groom Joanna R
Center for Immunology and Inflammatory Diseases, Division of Rheumatology, Allergy and Immunology, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02129, USA.
Luster Andrew D
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Article Info
Journal
Immunology and cell biology
Abbr.
Immunol Cell Biol
ISSN
1440-1711
DOI
10.1038/icb.2010.158
Published
2011-02-00
Epub
2011-00-11
Pages
207-15
Language
English
Region
United States
NLM ID
8706300
PMCID
PMC3863330
Subset
IM
Grants
NCI NIH HHS · R01 CA069212 · United States
External Links
PubMed source DOI: 10.1038/icb.2010.158 PMC Full Text View journal details
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