There have been several studies on macrophages involved in endometriosis. Let's look first at what, exactly, do macrophages do:
"Macrophages function as control switches of the immune system, providing a balance between pro-
"Macrophages are recruited at sites of hypoxia and tissue stress, where they clear cell debris and heme-iron and generate pro-life and pro-angiogenesis signals. Macrophages are abundant in endometriotic lesions, where are recruited and undergo alternative activation. In rodents macrophages are required for lesions to establish and to grow; bone marrow-derived Tie-2 expressing macrophages specifically contribute to lesions neovasculature, possibly because they concur to the recruitment of circulating endothelial progenitors, and sustain their survival and the integrity of the vessel wall. Macrophages sense cues (hypoxia, cell death, iron overload) in the lesions and react delivering signals to restore the local homeostasis: their action represents a necessary, non-redundant step in the natural history of the disease. Endometriosis may be due to a misperception of macrophages about ectopic endometrial tissue. They perceive it as a wound, they activate programs leading to ectopic cell survival and tissue vascularization. Clearing this misperception is a critical area for the development of novel medical treatments of endometriosis, an urgent and unmet medical need." http://www.ncbi.nlm.nih.gov/pubmed/23372570
"Macrophages particularly play important roles in facilitating development, growth, and repair of nerve fibers...Thus the evidence which suggests that the immune cell population, particularly macrophages, are likely to play crucial roles in growth and survival of nerve fibers in endometriosis is compelling, and indicates that certain inflammatory mechanisms may substantially contribute to the generation of pain in endometriosis." Endometriosis: Science and Practice edited by Linda C. Giudice, MD, Johannes L. H. Evers, MD, David L. Healy, MD http://books.google.com/books?id=kxzaBqmglrMC&pg=PA221...