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Related Collections Hemostasis, Thrombosis, and Vascular Biology Immunobiology Phagocytes Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 15 April 2001, Vol. 97, No. 8, pp. 2381-2389 IMMUNOBIOLOGY Apolipoprotein A-I inhibits the production of interleukin-1 and tumor necrosis factor- by blocking contact-mediated activation of monocytes by T lymphocytes Nevila Hyka, Jean-Michel Dayer, Christine Modoux, Tadahiko Kohno, Carl K. Edwards III, Pascale Roux-Lombard, and Danielle Burger Tumor necrosis factor- (TNF-) and interleukin-1 (IL-1), essential components in the pathogenesis of immunoinflammatory diseases, are strongly induced in monocytes by direct contact with stimulated T lymphocytes. This study demonstrates that adult human serum (HS) but not fetal calf or cord blood serum displays inhibitory activity toward the contact-mediated activation of monocytes by stimulated T cells, decreasing the production of both TNF- and IL-1. Fractionation of HS and N-terminal microsequencing as well as electroelution of material subjected to preparative electrophoresis revealed that apolipoprotein A-I (apo A-I), a "negative" acute-phase protein, was the inhibitory factor. Functional assays and flow cytometry analyses show that high-density lipoprotein (HDL)-associated apo A-I inhibits contact-mediated activation of monocytes by binding to stimulated T cells, thus inhibiting TNF- and IL-1 production at both protein and messenger RNA levels. Furthermore, apo A-I inhibits monocyte inflammatory functions in peripheral blood mononuclear cells activated by either specific antigens or lectins without affecting cell proliferation. These results demonstrate a new anti-inflammatory activity of HDL-associated apo A-I that might have modulating functions in nonseptic conditions. Therefore, because HDL has been shown to bind and neutralize lipopolysaccharide, HDL appears to play an important part in modulating both acute and chronic inflammation. The novel anti-inflammatory function of apo A-I reported here might lead to new therapeutic approaches in inflammatory diseases such as rheumatoid arthritis, multiple sclerosis, systemic lupus erythematosus, and atherosclerosis. © 2001 by The American Society of Hematology.   CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: J Frostegard Systemic lupus erythematosus and cardiovascular disease Lupus, May 1, 2008; 17(5): 364 - 367. [Abstract] [PDF] A. Scanu, N. Molnarfi, K. J. Brandt, L. Gruaz, J.-M. Dayer, and D. 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