Complement Protein C1q Enhances Macrophage Foam Cell Survival and Efferocytosis.

In the atherosclerotic lesion, macrophages ingest high levels of damaged modified low-density lipoproteins (LDLs), generating macrophage foam cells. Foam cells undergo apoptosis and, if not efficiently cleared by efferocytosis, can undergo secondary necrosis, leading to plaque instability and rupture. As a component of the innate immune complement cascade, C1q recognizes and opsonizes modified forms of LDL, such as oxidized or acetylated LDL, and promotes ingestion by macrophages in vitro.

Transcriptome data and gene ontology analysis in human macrophages ingesting modified lipoproteins in the presence or absence of complement protein C1q.

We characterized the transcriptional effects of complement opsonization on foam cell formation in human monocyte-derived macrophages (HMDM). RNA-sequencing was used to identify the pathways modulated by complement protein C1q during HMDM ingestion of the atherogenic lipoproteins oxidized low density lipoprotein (oxLDL) and acetylated low density lipoprotein (acLDL). All raw data were submitted to the MIAME-compliant database Gene Expression Omnibus (accession number GEO: GSE80442; http://www.

Macrophage molecular signaling and inflammatory responses during ingestion of atherogenic lipoproteins are modulated by complement protein C1q.

Background And Aims: This study investigated the effect of innate immune protein C1q on macrophage programmed responses during the ingestion of atherogenic lipoproteins. C1q plays a dual role in atherosclerosis where activation of complement by C1q is known to drive inflammation and promote disease progression. However, C1q is atheroprotective in early disease using mouse models.

Complement, c1q, and c1q-related molecules regulate macrophage polarization.

Complement is a critical system of enzymes, regulatory proteins, and receptors that regulates both innate and adaptive immune responses. Natural mutations in complement molecules highlight their requirement in regulation of a variety of human conditions including infectious disease and autoimmunity. As sentinels of the immune system, macrophages are specialized to respond to infectious microbes, as well as normal and altered self, and dictate appropriate immune responses.