The complement system is an important factor in innate immunity. The third complement component, C3, is central to the classical, alternative and lectin pathways of complement activation. The synthesis of C3 is tissue-specific and is modulated in response to a variety of stimulatory agents. During complement activation, C3 is proteolytically cleaved resulting in release of the anaphylatoxic peptide C3a. C3a is a small polypeptide consisting of 74aa (ca.10kD). C3a itself is very short-lived and in serum cleaved rapidly into the more stable C3a-desArg (also called acylation stimulating protein, ASP) . C3a exerts its function through a specific receptor (C3aR), which belongs to the G-protein coupled receptor family. Expression of C3aR has been reported in many cell types including myeloid and non-myeloid cells. Expression of C3aR on haematopoietic stem/progenitor cells has been shown to promote the trafficking/homing of these cells to the BM. Engagement of C3aR on DCs and T cells has been shown to up-regulate these cell functions. C3a is a mediator of local inflammatory processes. It induces smooth muscle contraction, increases vascular permeability, and causes histamine release from mast cells and basophilic leukocytes. C3a is involved in inflammatory reactions seen in gram-negative bacterial sepsis, trauma, ischemic heart disease, post-dialysis syndrome and a variety of autoimmune diseases. An inherited deficiency of C3 predisposes the person to frequent assaults of bacterial infections. In ulcerative colitis, and idiopathic chronic inflammatory bowel disease, the deposition of C3 in the diseased mucosa has been reported.