We have identified defects in phagocytosis by immune cells in both the brains and bodies of Fmr1 mutants, a Drosophila model of Fragile X Syndrome. Fragile X syndrome is the most common known monogenic cause of intellectual disability and autism, resulting from loss of an evolutionarily conserved translational inhibitor, Fmr1. Glia-mediated phagocytosis, the engulfment of extracellular material, is known to play an important role in neuronal structure and function but has not previously been implicated in neurodevelopmental diseases such as Fragile X syndrome. Here we investigate phagocytic immune cell function in Drosophila Fmr1 mutants. We show that Fmr1 mutants exhibit delays in phagocytosis by glia—both in the adult, after neuronal injury, and during neurodevelopment of the mushroom body, a brain structure required for learning and memory. In adults, the delay in phagocytosis is associated with a reduction in glial activation--specifically, expression of a crucial glial phagocytic receptor protein, Draper. We further demonstrate that these defects in phagocytosis are common to a second, developmentally independent lineage of blood immune cells in the body, or hemocytes. These results are the first demonstration of a defect in immune cell-mediated phagocytosis in any model of Fragile X Syndrome or autism and suggest the possibility that these defects contribute to the molecular mechanisms underlying neuronal dysfunction in these human diseases. .