Gut macrophages produce complement component C1q, which modulates neurogenic activity of gut peristalsis and is thus a key regulator of gastrointestinal motility.

Complement C1q directly drives the behavior of human neural stem cells via a classical receptor signaling mechanism modulating their capacity for functional integration in vivo.

The ability of C1q to bind to a variety of receptors has implications for signaling biology, spinal cord injury and, possibly, the evolution of the complement system.