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C1q and MBL, components of the innate immune system, influence monocyte cytokine expression
Author(s) -
Fraser Deborah A.,
Bohlson Suzanne S.,
Jasinskiene Nijole,
Rawal Nenoo,
Palmarini Gail,
Ruiz Sol,
Rochford Rosemary,
Tenner Andrea J.
Publication year - 2006
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.1105683
Subject(s) - biology , proinflammatory cytokine , immunology , innate immune system , immune system , acquired immune system , monocyte , cytokine , pattern recognition receptor , microbiology and biotechnology , inflammation
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)‐1α and IL‐1β, 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.