Immune-related vulnerabilities are commonly observed in those with SCZ (Muller et al., 2015). Maternal immune response to infectious agents have been causally implicated in individual risk for SCZ, particularly among individuals with a diathesis (Knuesel et al., 2014). Even ex-utero, exposure to infectious agents, such as Toxoplasmosis gondii, primarily transmitted to humans through fecal matter from infected carrier felines, precipitates onset of motor, psychotic, and cognitive symptoms (Torrey and Yolken, 2003, Sutterland et al., 2015). Antithetically, while individuals with schizophrenia are more likely to exhibit a pro-inflammatory phenotype (e.g., higher levels of cytokines), risk for rheumatoid arthritis, an autoimmune disorder is markedly reduced in those with schizophrenia and corresponds to a small, but significant, negative genetic correlation across the disorders as well (rg=−0.046) (Lee et al., 2015, Stringer et al., 2014, Euesden et al., 2015a). PRS may be particularly informative in studies exploring relationships with the immune system due to the overrepresentation of immune function loci in SCZ GWAS (Schizophrenia Working Group of the Psychiatric Genomics, 2014). For example, SCZ-PRS have been leveraged to test novel immune-related hypotheses with one
