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 Blood, 1 March 2008, Vol. 111, No. 5, pp. 2693-2703.
Prepublished online as a Blood First Edition Paper on December 19, 2007; DOI 10.1182/blood-2007-08-102319.

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IMMUNOBIOLOGY

Leukotriene B4 activates T cells that inhibit B-cell proliferation in EBV-infected cord blood–derived mononuclear cell cultures

Anquan Liu1, Hans-Erik Claesson2,3, Yilmaz Mahshid2, George Klein1, and Eva Klein1

1 Department of Microbiology, Tumor and Cell Biology, 2 Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm; and 3 Biolipox, Solna, Sweden

Epstein-Barr virus (EBV)–specific cellular memory is not transferred from mother to child. Therefore, EBV-induced B-cell proliferation in in vitro–infected cord blood mononuclear cell cultures is not inhibited. However, by addition of immunomodulators, polysaccharide K (PSK) or truncated thioredoxin (Trx80) that activate monocytes, EBV-specific T-cell response could be generated in such cultures. Presently, we demonstrate that leukotriene B4 (LTB4) is involved in the effect of the immunomodulators. LTB4 was detected in the medium, and T-cell activation was compromised by addition of leukotriene biosynthesis inhibitors. Moreover, we found that LTB4 added to infected cultures, which did not receive the immunomodulators, induced functional activation of the T cells. LTB4 activated the monocytes and acted directly on the T cells. In consequence, addition of LTB4 inhibited the EBV-induced proliferation of B lymphocytes. Specific cytotoxicity could be generated by restimulation of the T cells. The experiments showed successive stages of T-cell activation in acquisition of their immunologic effector function. This is orchestrated by complex cellular interactions, and autocrine loops mediated by soluble factors—here interferon (IFN)-{gamma}, interleukin (IL)-15, IL-12, and LTB4. Importantly, the results indicate that endogenous LTB4 can induce T-cell activation that inhibits the EBV-induced proliferation of B lymphocytes.


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