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Expression of lymphotoxin-ß on antigen-specific T cells is required for DC function

¹ Department of Immunology, University of Toronto, Toronto, Ontario, M5S 1A8 Canada
² Institute of Medical Microbiology, Universität Düsseldorf, D-40225 Düsseldorf, Germany

CORRESPONDENCE Jennifer Gommerman: jen.gommerman{at}utoronto.ca

During an immune response, activated antigen (Ag)-specific T cells condition dendritic cells (DCs) to enhance DC function and survival within the inflamed draining lymph node (LN). It has been difficult to ascertain the role of the tumor necrosis factor (TNF) superfamily member lymphotoxin-ß (LTß) in this process because signaling through the LTß-receptor (LTßR) controls multiple aspects of lymphoid tissue organization. To resolve this, we have used an in vivo system where the expression of TNF family ligands is manipulated only on the Ag-specific T cells that interact with and condition Ag-bearing DCs. We report that LTß is a critical participant required for optimal DC function, independent of its described role in maintaining lymphoid tissue organization. In the absence of LTß or CD40L on Ag-specific T cells, DC dysfunction could be rescued in vivo via CD40 or LTßR stimulation, respectively, suggesting that these two pathways cooperate for optimal DC conditioning.

Abbreviations used: FDC, follicular dendritic cell; HEV, high endothelial venule; HVEM, herpes virus entry mediator; LT, lymphotoxin; LTß, LT-ß; LTßR, LTß-receptor; SI, stimulation index; TRAF, TNF receptor–associated factor.

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