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Extra resources for Annual Review of Immunology Volume 23 2005

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HVEM-LIGHT Interactions on T Cells In Vitro Evidence that LIGHT binding to HVEM on T cells provides a costimulatory signal via HVEM signaling comes from several in vitro studies in which recombinant LIGHT protein or anti-HVEM immobilized with a suboptimal dose of anti-CD3 allows T cell proliferation, NF-κB activation, and/or cytokine production (37, 238, 243, 246, 247). Because the LTβR is absent from T cells, these effects of LIGHT can be attributed to LIGHT-HVEM interaction. Costimulatory effects of LIGHT on purified T cells are independent of CD28 signaling (246).

It is assumed that anti-4-1BB is directly expanding CD8 T cells in many of these models; however, there is also the possibility for effects of anti-4-1BB on NK cells and DC (215). In humans, the finding that 4-1BBL allows much better expansion of CD8 T cells than anti-CD3/CD28 alone (198) suggests that 4-1BBL stimulation will be useful in adoptive immunotherapy of cancer (235). HVEM/LIGHT The TNFR family member herpes virus entry mediator (HVEM) was first isolated as the receptor for herpes simplex virus 1 (HSV-1) (236).

Inclusion of 4-1BBL stimulation in cultures of anti-CD3/CD28-stimulated T cells results in substantial increases in recovery of T cells at 12–25 days of culture with minor effects on cell recoveries before 10 days (198). Thus 4-1BB ligation appears to be an important mediator of human CD8 T cell survival in vitro. Humans accumulate CD28− CD8 T cells with age or chronic infection (see references cited in 202), and human CD28− T cells are able to expand, develop effector function, and upregulate Bcl-XL in response to 41BBL costimulation (202, 208).

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