Trade-offs between reproduction and immunity are common among animals, potentially due to preferential allocation of limiting resources. In Drosophila melanogaster, mating increases egg production, but also triggers a rapid decrease in female immune defense. Here, I examine the dynamics of post-mating immune defense and identify how allocation of resources to oogenesis drives the trade-off between egg production and immunity.First, I found that mating continuously suppressed female immune defense for up to 10 days after mating as compared to age-matched unmated females. I additionally found that females mated either once or twice before infection survived at equal proportions, both with significantly lower probability than unmated females. I conclude that a single mating triggers a binary switch from mated to unmated state to persistently suppress the female immune system. Second, I hypothesized that direct resource allocation to yolk protein production and vitellogenesis limits female immune defense. I found that four mutants which arrest egg development prior to vitellogenesis maintain immune capacity after mating. I found that mating reduced the immune defense of okra females that complete vitellogenesis, but produce non-viable embryos. However, retained females, who complete egg development but do not oviposit, were not immune suppressed after mating. Additionally, I found that loss of yolk proteins increased immune performance relative to controls, but yolk protein mutants still experienced a reduction in immune capacity after mating. I conclude that production and incorporation of yolk proteins during sustained egg production limits female immune defense, but that other post-mating signaling mechanisms could also suppress immunity. Together, these results are consistent with the hypothesis that the dual demands of yolk protein production and immune defense places stress on the fat body, limiting timely and effective immune defense. Finally, I present evidence from collaborative projects investigating new potential genes involved in female immune defense and male reproduction. I find no evidence that dTCERG1, whose homolog inhibits immunity to promote reproduction in C. elegans, suppresses mated female D. melanogaster immune defense. I additionally found no evidence that dArc1, a gene annotated as regulating memory and metabolism and highly expressed in male accessory glands, influences competitive sperm fitness.