It was previously shown by our lab that mature phagolysosomes can transiently fuse with the plasma membrane and release their soluble contents into the extracellular milieu. This process, termed eructophagy, is believed to facilitate the spread of optimally stimulatory PAMPs and DAMPS to surrounding leucocytes. Our lab previously observed that neutrophils induce an increase in eructophagy in macrophages through direct contact. This was found to be dependent on ICAM-1 and LFA-1 on the surface of macrophages and neutrophils, respectively. The work presented in my thesis further explores the ICAM-1/LFA-1-dependent increase in macrophage eructophagy when in direct contact with vicinal leukocytes. I first observed that, similar to neutrophils, naive CD4+ T cells induce an increase in eructophagy in macrophages, dependent on ICAM-1 and LFA-1 on macrophages and T cells, respectively. To discern if ligation of ICAM-1 on its own increases eructophagy, I cross-linked ICAM-1 using antibodies and found that cross- linking of ICAM-1 was sufficient to induce eructophagy. Further, I showed that Lyn is necessary for induction of eructophagy downstream of ICAM-1. I explored the role of cortactin, a Lyn substrate, in the context of eructophagy. I found that eructophagy was not increased in cortactin knockdown macrophages in the presence of T cells, suggesting that cortactin could be acting downstream of ICAM-1 to induce increased eructophagy. Using phalloidin staining, I showed that F-actin structures appeared to differ significantly between cortactin knockdown and control macrophages, indicating that cortactin may be involved in the regulation of F-actin architecture at the cell cortex of macrophages. Overall, the work presented in this thesis suggests a novel pathway through which ICAM-1 signalling mediates increased eructophagy in macrophages. Taken togetherwith the previous observation that eructophagy activates vicinal leukocytes, the findings reported in this body of work suggest that eructophagy may allow for bidirectional communication between macrophages and surrounding leukocytes to amplify signals of inflammation in the local microenvironment.