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Article
Nature Immunology  4, 991 - 998 (2003)
Published online: 21 September 2003; | doi:10.1038/ni979

The inter-relatedness and interdependence of mouse T cell receptor big gammadelta+ and alphabold beta+ cells

Daniel J Pennington1, 4, Bruno Silva-Santos1, 4, John Shires1, 3, Efstathios Theodoridis1, Christopher Pollitt1, Emma L Wise1, Robert E Tigelaar2, Michael J Owen3 & Adrian C Hayday1

1  Peter Gorer Department of Immunobiology, Guy's King's Saint Thomas' Medical School, Guy's Hospital, London SE1 9RT, UK.

2  Department of Dermatology and Section of Immunobiology, Yale University, New Haven, Connecticut 06511, USA.

3  Present addresses: Department of Microbiology and Immunology, Emory University, Atlanta, Georgia 30322, USA (J.S.) and GlaxoSmithKline, Medicines Research Centre, Gunnels Wood Road, Stevenage, Hertfordshire SG1 2NY, UK (M.J.O.).

4  These authors contributed equally to this work.

Correspondence should be addressed to Adrian C Hayday adrian.hayday@kcl.ac.uk
Although T cell receptor (TCR)bold gammadelta+ and TCRalphabeta+ cells are commonly viewed as functionally independent, their relatedness and potential interdependence remain enigmatic. Here we have identified a gene profile that distinguishes mouse bold gammadelta cell populations from conventional alphabeta T cells. However, this profile was also expressed by sets of unconventional alphabeta T cells. Therefore, whereas TCR specificity determines the involvement of a T cell in an immune response, the cell's functional potential, as assessed by gene expression, does not segregate with the TCR. By monitoring the described gene profile, we show that bold gammadelta T cell development and function in TCRbeta-deficient mice was impaired because of the absence of alphabeta T cell progenitors. Thus, normal bold gammadelta cell development is dependent on the development of conventional alphabeta T cells.

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Nature Immunology
ISSN: 1529-2908
EISSN: 1529-2916
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