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Blood, 15 May 2007, Vol. 109, No. 10, pp. 4328-4335.
Prepublished online as a Blood First Edition Paper on January 25, 2007; DOI 10.1182/blood-2006-12-064170.
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IMMUNOBIOLOGY
TCR dimlymphocytes define populations of circulating effector cells that migrate to inflamed tissues
Zhuoli Zhang1,
Claire L. Gorman1,
Anna-Chiara Vermi1,
Claudia Monaco1,
Andrew Foey1,
Sally Owen1,
Parisa Amjadi1,
Alena Vallance1,
Catherine McClinton1,
Federica Marelli-Berg2,
Pia Isomäki1,
Andrew Russell2,
Francesco Dazzi2,
Timothy J. Vyse2,
Fionula M. Brennan1, and
Andrew P. Cope1
1 Kennedy Institute of Rheumatology Division and
2 Division of Medicine, Faculty of Medicine, Imperial College London, United Kingdom
The T-cell receptor  (TCR) chain is a master sensor and regulator of lymphocyte responses. Loss of TCR expression has been documented in infectious, inflammatory, and malignant diseases, suggesting that it may serve to limit T-cell reactivity and effector responses at sites of tissue damage. These observations prompted us to explore the relationship between TCR expression and effector function in T cells. We report here that TCRdim lymphocytes are enriched for antigen-experienced cells refractory to TCR-induced proliferation. Compared to their TCRbright counterparts, TCRdim cells share characteristics of differentiated effector T cells but use accessory pathways for transducing signals for inflammatory cytokine gene expression and cell contact-dependent pathways to activate monocytes. TCRdim T cells accumulate in inflamed tissues in vivo and have intrinsic migratory activity in vitro. Whilst blocking leukocyte trafficking with anti-TNF therapy in vivo is associated with the accumulation of TCRdim T cells in peripheral blood, this T-cell subset retains the capacity to migrate in vitro. Taken together, the functional properties of TCRdim T cells make them promising cellular targets for the treatment of chronic inflammatory disease.
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