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Compared to the successes achieved through GWAS of common inflammatory and autoimmune traits, equivalent GWAS for infectious disease susceptibility determinants have identified fewer novel associations. These apparent shortcomings can be attributed to multiple reasons including differential exposure to infectious agents, substantial microbial heterogeneity and diverse population structures in those populations suffering the greatest burden of infectious disease. In this talk I will discuss approaches used in our lab to build upon these observations using antibody profiling of responses to infections as proxy markers of infectious disease. By applying multiplexed, scalable methods to even modest sample sizes by modern standards we are able to identify a range of genetic signals that we can further demonstrate to be highly relevant to disease. Furthermore, through knowing the specific antigens driving these associations we can harness these signals to further our understanding of disease susceptibility to molecular mechanistic levels. I will finally discuss the implications that these findings will have towards improving human health.