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Endometriosis (EM) is defined as the engraftment and proliferation of functional endometrial-like tissue outside the uterine cavity that lead to a chronic inflammatory condition. Even if the aetiology of EM remains unclear, numerous recent studies underlined the pivotal role of a dysfunctional immune system and the complement system (CS) is one of the predominant altered pathways. Among the complement proteins that are synthesized locally, the first effector molecule of the classical pathway, C1q, takes centre stage for its central roles in several processes independent of complement activation, such as tumour growth, placentation and wound-healing angiogenesis. Gene expression analysis of C1q in EM tissues and cells isolated from patients enrolled at the Institute for Maternal and Child Health "Burlo Garofolo" in Trieste (ITALY), revealed a high level of C1q expression in all samples. The presence of C1q protein in EM tissues has been confirmed by immunohistochemical analysis, identifying macrophages as likely local producers. Subsequently, to investigate a possible modulation of the C1q expression induced by the EM milieu, patient macrophages were stimulated with a conditioned medium (CM) of endometriotic cells. We demonstrated that the CM of endometriotic cells was able to induce up-regulation of C1q gene expression by macrophages. Consequently, to better investigate why C1q expression was increased in endometriosis, we focus on its known pro-angiogenic role. Performing several angiogenesis assays on primary endothelial endometriotic cells, such as migration, proliferation and tube formation assays, we observed a strong pro-angiogenic effect induced by C1q on EM endothelial cells. [ABSTRACT FROM AUTHOR]