Mammary gland involution is marked by extensive apoptotic cell death of the secretory, mammary epithelial cells. This death is physiologic, and the removal of the apoptotic cells is anti-inflammatory and anti-immunogenic under healthy conditions. The mechanisms used by mammary epithelial cells during the engulfment of apoptotic cells were explored in this thesis. For these studies, an in vitro model system was designed utilizing the mammary epithelial cell line, EpH4 cells, as the phagocyte. Apoptotic, mammary epithelial cells were harvested from the mammary gland during involution and used as the apoptotic target for our studies, Through direct comparison to J774 macrophages, it was demonstrated that EpH4 cells engulfed milked, apoptotic cells as efficiently as professional phagocytes. It was shown that the downstream mediators of phagocytosis such as actin polymerization, PI3K-, and PKCδ-activation were all used by EpH4 cells. Previously termed efferocytosis, it was discovered that a macropinocytosis-like mechanism of phagocytosis was employed during the engulfment of milked, apoptotic cells. In this, EpH4 cell phagocytosis was sensitive to amiloride and was enhanced with the inhibition of RhoA. Through inhibitors and knockout mice, it was found that the receptor recognition system applied by EpH4 cells included the receptors Lrp-1, Alpha v integrins, and Mer. Additionally, the ligands on milked, apoptotic cells important for their removal included the opsonizing proteins MFG-E8 and sCD14, and PtdSer exposure. Two novel mechanisms were discovered to regulate the phagocytic competency of mammary epithelial cells including target specificity and the availability of phagocytic receptors. The in vitro phagocytic potential of EpH4 cells was revealed when the targets more closely resembled an in vivo target and was an apoptotic mammary epithelial cell or the target was pre-incubated in milk. Pre-incubation in murine milk increased the permeability of these targets, changed the size, and increased the opsonizing proteins on the targets. TGFβ was found to activate phagocytic competency in polarized EpH4 cells. TGFβ was able to mediate these effects by altering tight junction integrity. This allowed for the apical localization of the phagocytic receptors, Mer, Alpha v integrins, and Lrp-1 putting the receptors in contact with apoptotic targets.