|
|
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.
Previous Article | Next Article 
Submitted December 20, 2006
Accepted January 16, 2007
TCR dim lymphocytes define populations of circulating effector cells that migrate to inflamed tissues
Zhuoli Zhang, Claire L Gorman, Anna-Chiara Vermi, Claudia Monaco, Andrew Foey, Sally Owen, Parisa Amjadi, Alena Vallance, Catherine McClinton, Federica M. Marelli-Berg, Pia Isomaki, Andrew Russell, Francesco Dazzi, Timothy J Vyse, Fionula M Brennan, and Andrew P Cope*
The Kennedy Institute of Rheumatology Division, Imperial College, London, United Kingdom
Division of Medicine, Imperial College, London, United Kingdom
* Corresponding author; email: andrew.cope{at}imperial.ac.uk.
The T cell receptor zeta (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 TCR dim lymphocytes are enriched for antigen experienced cells refractory to TCR-induced proliferation. Compared to their TCR bright counterparts, TCR dim cells share characteristics of differentiated effector T cells but utilise accessory pathways for transducing signals for inflammatory cytokine gene expression, and cell contact dependent pathways to activate monocytes. TCR dim T cells accumulate in inflamed tissues in vivo and have intrinsic migratory activity in vitro. Whilst blocking leucocyte trafficking with anti-TNF therapy in vivo is associated with the accumulation of TCR dim T cells in peripheral blood, this T cell subset retains the capacity to migrate in vitro. Taken together, the functional properties of TCR dim T cells make them promising cellular targets for the treatment of chronic inflammatory disease.

CiteULike Connotea Del.icio.us Digg Reddit Technorati What's this?
This article has been cited by other articles:

|
 |

|
 |
 
J. R. F. Abreu, A. M. Grabiec, S. Krausz, R. Spijker, T. Burakowski, W. Maslinski, E. Eldering, P. P. Tak, and K. A. Reedquist
The Presumed Hyporesponsive Behavior of Rheumatoid Arthritis T Lymphocytes Can Be Attributed to Spontaneous Ex Vivo Apoptosis rather than Defects in T Cell Receptor Signaling
J. Immunol.,
July 1, 2009;
183(1):
621 - 630.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
E. Ammirati, A.-C. Vermi, D. Cianflone, M. Banfi, C. Foglieni, C. Godino, F. Airoldi, L. A. Ferri, C. L. Gorman, A. A. Manfredi, et al.
Expansion of T-Cell Receptor {zeta}dim Effector T Cells in Acute Coronary Syndromes
Arterioscler Thromb Vasc Biol,
December 1, 2008;
28(12):
2305 - 2311.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
J. D. Isaacs
Therapeutic T-cell manipulation in rheumatoid arthritis: past, present and future
Rheumatology,
October 1, 2008;
47(10):
1461 - 1468.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
A. Das, M. Hoare, N. Davies, A. R. Lopes, C. Dunn, P. T.F. Kennedy, G. Alexander, H. Finney, A. Lawson, F. J. Plunkett, et al.
Functional skewing of the global CD8 T cell population in chronic hepatitis B virus infection
J. Exp. Med.,
September 1, 2008;
205(9):
2111 - 2124.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
C. L. Gorman, A. I. Russell, Z. Zhang, D. Cunninghame Graham, A. P. Cope, and T. J. Vyse
Polymorphisms in the CD3Z Gene Influence TCR{zeta} Expression in Systemic Lupus Erythematosus Patients and Healthy Controls
J. Immunol.,
January 15, 2008;
180(2):
1060 - 1070.
[Abstract]
[Full Text]
[PDF]
|
 |
|
|
|