Accuri C6 Flow Cytometer System
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© by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.1007701

Received for publication October 21, 2007.
Revised February 15, 2008.
Accepted for publication February 18, 2008.

Article

Cytokines secreted by IL-2-activated lymphocytes induce endogenous nitric oxide synthesis and apoptosis in macrophages

Kyoung-Seong Choi *, Eun-Kee Song {dagger}, and Chang-Yeol Yim {dagger}@

*Department of Animal Science, Kyungpook National University, Sangju, Republic of Korea; and {dagger}Department of Internal Medicine, Chonbuk National University Medical School, Research Institute of Clinical Medicine, and Advanced Research Cancer Center, Chonbuk National University Hospital, Chonju, Chonbuk, Republic of Korea

@ To whom correspondence should be addressed. E-mail: cyyim{at}chonbuk.ac.kr.


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Abstract

IL-2-activated killer (LAK) cells secrete inflammatory cytokines such as IFN-{gamma} and TNF-{alpha}, which can induce NO synthesis (NOS). In this study, we investigated IL-2-activated, lymphocyte-mediated macrophage apoptosis via NOS. LAK cells and their culture supernatants induced NOS in murine macrophages. NOS was markedly inhibited by blocking antibodies to IFN-{gamma} and TNF-{alpha}, suggesting the key role of these lymphocyte cytokines in mediating NOS. Endogenous NO production inhibited macrophage proliferation and induced apoptosis in concordance with p53 accumulation and caspase-3 activation, processes that were inhibited by NG-monomethyl-L-arginine (a NOS inhibitor) and 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl 3-oxide (a NO scavenger). Our study demonstrated a novel, noncontact-dependent mechanism of macrophage suppression by IL-2-activated lymphocytes: induction of growth inhibition and apoptosis of macrophages as a result of endogenous NOS induced by cytokines secreted from IL-2-activated lymphocytes.

Key Words: programmed cell death • iNOS • carboxy-PTIO • SNAP • p53 • caspase-3




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