Vaccines provide protection from pathogens by eliciting high affinity, neutralizing antibody responses through germinal center (GC) reactions. Within GCs, T follicular helper (Tfh) cells orchestrate the selection of affinity-matured memory B cells and long-lived plasma cells. With the emergence of the COVID-19 pandemic, the utility of the messenger RNA (mRNA) vaccine platform has become increasingly evident due to its ease of adaptability to target emerging viral variants as well as its ability to drive potent humoral responses. Data from our group has shown that these potent humoral immune responses correlate with a robust induction of Tfh cells, however, the mechanism of Tfh induction by mRNA vaccines is largely unknown. Most mRNA vaccines consist of nucleoside-modified mRNA encoding the antigen-of-interest encapsulated in lipid nanoparticles (LNPs), which protect the mRNA from degradation and allow for its delivery into the cytosol. Herein, we have uncoupled distinct, yet complimentary, roles for both the LNP and nucleoside-modified mRNA in promoting Tfh cell responses. We demonstrated that LNPs are robust Tfh cell inducing adjuvants when combined with protein antigens in the absence of mRNA through a mechanism that is heavily reliant on the local production of IL-6 within the draining lymph nodes (dLNs). Through a proximity dependent labeling (LIPSTIC) approach coupled with single-cell transcriptomic analysis, we additionally discovered that LNPs drive broad activating effects on type-2 conventional dendritic cells (cDC2s) within the dLN irrespective of T cell help, which included the upregulation of a “pro-Tfh cell” program. Interestingly, when we interrogated the quality of the immune response driven by both LNPs and nucleoside-modified mRNAs, we found that LNPs favored a Th2- biased Tfh cell response while nucleoside-modified mRNAs drove a Th1-biased response. Upon further interrogation, we discovered that this Th1-bias driven by nucleoside-modified mRNA was dependent on type I interferons which acted directly on DCs to drive their maturation and increase the magnitude of GC responses. Taken together, we believe that the information gleaned from these studies will begin to unravel the mechanism by which mRNA vaccines induce Tfh cells, providing critical information for the rational design of vaccines against hard-to-neutralize pathogens.