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 Blood, 15 January 2009, Vol. 113, No. 3, pp. 622-625.
Prepublished online as a Blood First Edition Paper on November 20, 2008; DOI 10.1182/blood-2008-03-139964.

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IMMUNOBIOLOGY

Brief report

Impaired negative regulation of homeostatically proliferating T cells

Anna Shvets1,*, Rabindranath Chakrabarti1,*, Rosana Gonzalez-Quintial2, Roberto Baccala2, Argyrios N. Theofilopoulos2, and Gérald J. Prud'homme1

1 Department of Laboratory Medicine, St Michael's Hospital and University of Toronto, Toronto, ON; and 2 Department of Immunology, IMM-3, The Scripps Research Institute, La Jolla, CA

Acute lymphopenia-induced homeostatic proliferation (HP) of T cells promotes antitumor immunity, but the mechanism is unclear. We hypothesized that this is due to a lack of inhibitory signals that allows activation of T cells with low affinity for self-antigens. Tumors resist immunity in part by expressing inhibitory molecules such as PD-1 ligand 1 (PD-L1), B7-H4, and TGF-β. In irradiated mice undergoing HP, we found that T cells displayed a severe deficit in the activation-induced expression of inhibitory molecules PD-1 and CTLA-4, and TGF-β1–induced expression of Foxp3. HP T cells were also less suppressed by B7-H4/Ig and, unlike control T cells, failed to produce IL-10 in response to this molecule. This deficiency in regulation was reversed as normal T-cell numbers were restored. We conclude that T cells are weakly regulated by inhibitory molecules during the acute phase of HP, which could explain their increased effectiveness in cancer immunotherapy.


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