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Published online before print April 14, 2006
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,2
* Departments of Molecular Biology and Biochemistry and
Pathology, Center for Immunology, University of California, Irvine;
Department of Biochemistry, University of Texas Health Center at Tyler; and
Department of Microbiology and Immunology, State University of New York, Upstate Medical University, Syracuse
2 Correspondence: Departments of Molecular Biology and Biochemistry and Pathology, Center for Immunology, 3205 McGaugh Hall, University of California, Irvine, CA 92697. E-mail: ATenner{at}uci.edu
It has recently been recognized that the innate immune response, the powerful first response to infection, has significant influence in determining the nature of the subsequent adaptive immune response. C1q, mannose-binding lectin (MBL), and other members of the defense collagen family of proteins are pattern recognition molecules, able to enhance the phagocytosis of pathogens, cellular debris, and apoptotic cells in vitro and in vivo. Humans deficient in C1q inevitably develop a lupus-like autoimmune disorder, and studies in C1q knockout mice demonstrate a deficiency in the clearance of apoptotic cells with a propensity for autoimmune responses. The data presented here show that under conditions in which phagocytosis is enhanced, C1q and MBL modulate cytokine production at the mRNA and protein levels. Specifically, these recognition molecules of the innate immune system contribute signals to human peripheral blood mononuclear cells, leading to the suppression of lipopolysaccharide-induced proinflammatory cytokines, interleukin (IL)-1
and IL-1ß, and an increase in the secretion of cytokines IL-10, IL-1 receptor antagonist, monocyte chemoattractant protein-1, and IL-6. These data support the hypothesis that defense collagen-mediated suppression of a proinflammatory response may be an important step in the avoidance of autoimmunity during the clearance of apoptotic cells.
Key Words: human • macrophages • complement
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