Nitrogen is essential for plant tissue growth but is often a limited resource in soils. Many legumes overcome this limitation by entering a symbiotic association with soil microbes, called rhizobia, which provide nitrogen to the plant while rhizobia receive fixed carbon. To successfully form a symbiosis, the host and symbiont exchange a series of molecular signals. One major obstacle during this interaction is the host's innate immune system, which becomes active upon rhizobial detection. It is therefore the main focus of this thesis to identify the mechanisms that modulate host immunity. In the subsequent chapters, we focus on a rhizobial mechanism of defense response evasion relevant in early stages of root infection, and a later stage, nodule-specific mechanism of host defense response suppression. Here, we demonstrated that the abundantly expressed rhizobial exopolysaccharide-I (EPS-I) of Sinorhizobium meliloti provided a survival advantage in the Medicago truncatula mutant, called defective in nitrogen fixation 2 (dnf2) which exhibits enhanced host defenses in nodules. We then determined that rhizobial EPS-I provided protection against MAMP-triggered immune defenses activated by host pattern recognition receptors of the plant family of LysM domain-containing proteins, called LYM1 and LYM2. We determined that the underlying mechanism of protection conferred by EPS-I was the suppression of the reactive oxygen species burst upon detection of rhizobia. In addition, we provided insight into the nodule-specific mechanism of host defense suppression during nodule cell invasion by rhizobia. We showed that inactive LYM1 and LYM2 proteins within nodules of the dnf2 mutant allowed for the progression of infection by rhizobia.