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Blood, 15 February 2005, Vol. 105, No. 4, pp. 1606-1613. Prepublished online as a Blood First Edition Paper on October 26, 2004; DOI 10.1182/blood-2004-06-2406.
Submitted June 24, 2004
Microbiology and Tumor Biology Center, Karolinska Institute, Stockholm, Sweden * Corresponding author; email: Anquan.Liu{at}mtc.ki.se.
EBV specific immunological memory is not transferred from mother to child. In vitro infection of cord blood cells can therefore readily lead to the outgrowth of transformed B lymphocytes. We found that the immunomodulator PSK or the mitogenic cytokine Trx80 inhibited the EBV induced B cell proliferation. Using SAP induction as a sign for T, NK cell activation we could follow it without any need for cell separation because neither macrophages nor B lymphocytes express SAP. The results suggest the following scenario: EBV infected and activated B lymphocytes. They were recognized by T cells that became posed for responding to cytokines produced by monocytes. PSK and Trx80, which is a secreted C-terminally truncated thioredoxin, both activated the monocytes which then produced cytokines in the presence of the primed T cells. PSK induced IL-15 while Trx80 induced IL-12 production. Both cytokines activated the T cells for function. PI 3-kinase and ROS were involved in the PSK induced activation of monocytes. Restimulation of the cultures with EBV transformed B cells generated specific cytotoxic activity.
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