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Proc Natl Acad Sci U S A
1997 Oct 14;9421:11514-9. doi: 10.1073/pnas.94.21.11514.
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MIC-1, a novel macrophage inhibitory cytokine, is a divergent member of the TGF-beta superfamily.
Bootcov MR
,
Bauskin AR
,
Valenzuela SM
,
Moore AG
,
Bansal M
,
He XY
,
Zhang HP
,
Donnellan M
,
Mahler S
,
Pryor K
,
Walsh BJ
,
Nicholson RC
,
Fairlie WD
,
Por SB
,
Robbins JM
,
Breit SN
.
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Macrophages play a key role in both normal and pathological processes involving immune and inflammatory responses, to a large extent through their capacity to secrete a wide range of biologically active molecules. To identify some of these as yet not characterized molecules, we have used a subtraction cloning approach designed to identify genes expressed in association with macrophage activation. One of these genes, designated macrophage inhibitory cytokine 1 (MIC-1), encodes a protein that bears the structural characteristics of a transforming growth factor beta (TGF-beta) superfamily cytokine. Although it belongs to this superfamily, it has no strong homology to existing families, indicating that it is a divergent member that may represent the first of a new family within this grouping. Expression of MIC-1 mRNA in monocytoid cells is up-regulated by a variety of stimuli associated with activation, including interleukin 1beta, tumor necrosis factor alpha (TNF-alpha), interleukin 2, and macrophage colony-stimulating factor but not interferon gamma, or lipopolysaccharide (LPS). Its expression is also increased by TGF-beta. Expression of MIC-1 in CHO cells results in the proteolytic cleavage of the propeptide and secretion of a cysteine-rich dimeric protein of Mr 25 kDa. Purified recombinant MIC-1 is able to inhibit lipopolysaccharide -induced macrophageTNF-alpha production, suggesting that MIC-1 acts in macrophages as an autocrine regulatory molecule. Its production in response to secreted proinflammatory cytokines and TGF-beta may serve to limit the later phases of macrophage activation.
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