Phagocytosis is a fundamental and evolutionarily conserved process. It plays a role in both homeostasis and host defense by the removal of apoptotic cells and pathogens, respectively. There are several receptors expressed by phagocytic cells that recognize apoptotic cells and pathogens. One such receptor family is the Nimrod (Nim) proteins. We know from the previous studies, that several Nimrod C-type proteins are involved in the phagocytosis process of bacteria or apoptotic cells (Eater and NimC1, Draper and NimC4/SIMU, respectfully). To date, the role of the NimB-type proteins remains poorly understood. Two secreted Nim proteins (NimB4 and NimB5) have recently been characterized. NimB4 plays a role as a bridging molecule in phagocytosis while NimB5 regulates hemocyte proliferation and adhesion. In this research project, we aim to characterize the functions of another member of the Nimrod family in Drosophila immunity, of the secreted NimB1 protein. Our preliminary data show, that NimB1 may have similar roles to that of NimB4 and NimB5. Similar to NimB4, NimB1 is secreted by hemocytes and it binds to apoptotic cells. Moreover, the NimB1 mutant presents enlarged phagosomes, suggesting a defect in phagosome formation. However, we did not find defects in the phagocytosis of apoptotic cells with our in-vitro experiments with the third instar larval hemocytes. Interestingly, we showed, that like NimB5, NimB1 is also able to regulate macrophage number and influence their adhesion properties.