Complement component 1q (C1q) is the recognition molecule of the classical pathway of the
complement system that can bind to an array of closely spaced antigen-bound immunoglobulin G (IgG)
and IgM antibodies. In addition to its involvement in defence against a range of pathogens and clearance
of apoptotic and necrotic cells, C1q has also been implicated in immune and non-immune homeostasis.
C1q is locally produced by immune cells such as monocytes, macrophages, and dendritic cells. C1q is also
synthesized by decidual endothelial cells, thus acting as a link between decidual cells and trophoblasts,
as well as contributing to the remodelling of spiral arteries. Furthermore, C1q is produced by the
extravillous trophoblasts (EVTs) invading the decidua. As a pro-angiogenic molecule, C1q is also important
for normal placentation processes as it favors the active angiogenesis in the developing decidua. These
observations have been validated by C1q gene knock-out mice which showed pre-eclampsia (PE)-like
symptoms, characterized by hypertension, proteinuria, glomerular endotheliosis, and increased soluble
fms-like tyrosine kinase-1 (sFlt-1)/placental growth factor (PlGF) ratio, and increased oxidative stress.
The role of C1q in normal and adverse human pregnancy is being studied extensively due to its absence or
low level as a likely precipitating factor for the development of PE.
