Journal
JOURNAL OF CLINICAL INVESTIGATION
Volume 107, Issue 5, Pages 595-601Publisher
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI11902
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Funding
- NIAID NIH HHS [N01AI40034, 5T32 AI-07328, V19 AI-40034, T32 AI007328] Funding Source: Medline
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Chemokine receptor expression is finely controlled during T-cell development. We show that newly identified chemokine receptor Bonzo/CXCR6 is expressed by subsets of Th1 or T-cytotoxic 1 (Tc 1) cells, but not by Th2 or Tc2 cells, establishing Bonzo as a differential marker of polarized type 1 T cells in vitro and in vivo. Priming of naive T cells by dendritic cells induces expression of Bonzo on T cells. 1L-12 enhances this dendritic cell-dependent upregulation, while IL-4 inhibits it. In blood, 35-56% of Bonzo(+) CD4 T cells are Th1 cells, and 60-65% of Bonzo(+) CD8 T cells are Tc1 cells, while few Bonzo(+) cells are type 2 T cells. Almost all Bonzo(-) Tc1 cells contain preformed granzyme A and display cytotoxic effector phenotype. Most Bonzo(+) T cells lack L-selectin and/or CCR7, homing receptors for lymphoid tissues. Instead, Bonzo(+) T cells are dramatically enriched among T cells in tissue sites of inflammation, such as rheumatoid joints and inflamed livers. Bonzo may be important in trafficking of effector T cells that mediate type 1 inflammation, making it a potential target for therapeutic modulation of inflammatory diseases.
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