The decline of cognitive function has emerged as one of the greatest health threats of old age. Age-related cognitive decline is caused by an impacted neuronal circuitry, yet the molecular mechanisms responsible are unknown. C1q, the initiating protein of the classical complement cascade and powerful effector of the peripheral immune response, mediates synapse elimination in the developing CNS....

Complement C1q is the first subcomponent of the classical complement pathway, and a major molecule connecting link between innate and adaptive immunity. Mammalian C1q is a hexamer of a molecular weight about 410 kDa; however, little is known about its structural characteristics in teleost. In this study, a rapid method for isolation of the C1q (OnC1q) was developed to investigate its biochemica...

The first step in the activation of the classical complement pathway by immune complexes involves the binding of the six globular heads of C1q to the Fc regions of IgG or IgM. The globular heads of C1q (gC1q domain) are located C-terminal to the six triple-helical stalks present in the molecule, each head being composed of the C-terminal halves of one A, one B, and one C chain. The gC1q modules...

OBJECTIVE Activation of the complement system plays a key role in inflammation associated with vascular injury. Recently, platelet P-selectin was shown to activate C3 via the alternative pathway of human complement. As platelets also posses binding sites for C1q, the recognition unit of the classical complement pathway, the present study examined classical pathway activation on platelets. MET...

BACKGROUND Complement functions as an important host defense system and complement C5 and C7 have been implicated in immunopathology of tuberculosis. However, little is known about the role of other complement components in tuberculosis. METHODS Complement gene expression in peripheral blood mononuclear cells of tuberculosis patients and controls were determined using whole genome transcripti...

Objectives. The study was conducted to determine the correlation of ICAM-1, VCAM-1, and anti-C1q antibody levels with SLE disease activity index (SLEDAI) and standard SLE disease activity immunological markers (anti-dsDNA and sera C3 and C4). Study Design. This was a cross-sectional study. Materials and Methods. Blood samples were obtained from 95 SLE patients (45 active SLE and 50 nonactive SL...

C1q, the recognition subunit of the C1 complex of complement, is an archetypal pattern recognition molecule with the striking ability to sense a wide variety of targets, including a number of altered self-motifs. The recognition properties of its globular domain were further deciphered by means of x-ray crystallography using deoxy-D-ribose and heparan sulfate as ligands. Highly specific recogni...

During development, the formation of mature neural circuits requires the selective elimination of inappropriate synaptic connections. Here we show that C1q, the initiating protein in the classical complement cascade, is expressed by postnatal neurons in response to immature astrocytes and is localized to synapses throughout the postnatal CNS and retina. Mice deficient in complement protein C1q ...

We read with interest the report of Marto et al on the occurrence of anti-C1q antibodies in systemic lupus erythematosus (SLE), particularly their finding of anti-C1q in 39.8% of patients with SLE without renal disease, 27.3% of whom went on to develop nephritis. We recently tested for anti-C1q antibodies using an enzyme linked immunosorbent assay (ELISA) kit (Buhlmann Laboratories, Basel) in t...

Microglial activation has been associated with several degenerative diseases of the central nervous system (CNS). One consequence of activation is the induction of a more efficient phagocytic response, and it is therefore important to determine what factors regulate microglial phagocytosis and whether this capacity influences the progression of neurodegenerative changes. Previous studies have d...