The endometriotic disease process is associated with a perturbed immunological profile including increased activity of regulatory T cells, which potentially facilitate the survival of shed endometrial fragments in endometriosis. Upstream regulators of T lymphocytes are antigen-presenting cells (APCs) including macrophages and dendritic cells. We hypothesised that altered function of APCs might be apparent in the eutopic endometrium and this would be reflected in dysregulated transcription of APC immune-regulatory genes in women with endometriosis. Twenty-nine genes encoding surface markers and cytokines associated with APC recruitment and/or functional activation were evaluated in eutopic endometrium from women with (n=22) and without endometriosis (n=20) during both proliferative and secretory phases. RNA was extracted using miRNeasy kit, and the genes were quantified using RT-qPCR. The Mann-Whitney U test was applied to ΔΔCt values. Most notably, we found the expression of key APC-regulatory genes TGFβ3 and NGF encoding transforming growth factor-β3 and nerve growth factor are significantly higher in women with endometriosis than control women during the secretory phase. Expression of IDO which encodes indolamine 2,3-dioxygenase, a marker of tolerogenic dendritic cells, was up-regulated after ovulation to a higher extent in women with endometriosis. Dysregulated expression of CCL2 encoding macrophage chemotactic protein-1 was also evident in women with endometriosis in the secretory phase. The other 20 genes of interest showed comparable levels between both groups in both menstrual cycle phases. These results are consistent with the conclusion of altered dendritic cell and macrophage phenotype and potentially elevated tolerogenic function in the eutopic endometrium of women with endometriosis.