In response to infection or immunization, antibodies are produced that provide protection against re-exposure with the same pathogen. These antibodies can persist at high titers for decades and are maintained by bone marrow-resident long-lived plasma cells (LLPC). However, the durability of antibody responses to immunization varies amongst vaccines. It is unknown what factors contribute to the differential longevity of serum antibody responses and whether heterogeneity in LLPC contributes to this phenomenon. While LLPC differentiation has been studied extensively in mice, little is known about this population in humans or non-human primates (NHP). Here, we use multi-omic single-cell profiling to identify and characterize the LLPC compartment in NHP. We identify LLPC biomarkers including the marker CD102 and show that CD102 in combination with CD31 identifies LLPC in NHP bone marrow. Additionally, we find that CD102 is expressed by LLPC in mouse and humans. These results further our understanding of the LLPC compartment in NHP, identify biomarkers of LLPC, and provide tissue-specific single cell references for future studies.

Adjuvants boost the immune response to vaccine antigens, serving as key components in safe and effective vaccines. However, selecting a suitable adjuvant for a new vaccine can be challenging. This is due to the wide variety of adjuvants and the many mechanisms of vaccines they are meant to enhance. Therefore, the adjuvant selection process heavily relies on empirical experiments, which are time-consuming and resource-intensive. In this study, we introduce a machine learning approach leveraging non-human primate RNA transcriptomic data to predict immunogenic antibody levels after vaccination. Furthermore, analysis of the trained deep learning models enabled the identification of immune response mechanisms that are stimulated by adjuvants. Integration of machine learning has the potential to expedite vaccine adjuvant selection by focusing on evaluating adjuvant candidates with the highest probability of success. This may ultimately facilitate the development of more effective vaccines.

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Long-lived plasma cells (LLPCs) are a subset of antibody secreting cells (ASCs) that reside within lymphoid tissues, including the bone marrow (BM) and gut associated lymphoid tissues (GALT), and can secrete antigen-specific antibodies for up to decades or longer. Due to these traits, LLPCs serve as a crucial mediator for durable protective immunity. The signals needed to control the differentiation of LLPCs from naïve B cells, however, are not well understood. Accordingly, it remains a challenge to design vaccines that specifically drive LLPC generation and subsequent antibody durability. In this review, we discuss LLPC generation and heterogeneity following vaccination, vaccine design decisions known to impact immunological memory, and how novel emerging technologies can be used to inform on LLPC biology to enable LLPC targeting vaccine design.

Background/Objectives: Adjuvants, added to vaccines to enhance immune responses, are central to shaping the magnitude and durability of immunity, yet their precise mechanisms remain incompletely defined. This study evaluated how diverse adjuvant combinations influence HPV vaccine immunogenicity in non-human primates, with a particular focus on impacts on hematopoietic biology—megakaryocytes and platelets—and broader innate and adaptive pathways. Methods: Eight adjuvanted formulations, each incorporating distinct immunomodulatory components and delivery platforms, were compared against an alum-only control in non-human primates. Longitudinal antibody titers (HPV16-specific) were measured up to 54 weeks, and blood transcriptomes were profiled at Day 1 and Day 7 after both prime and boost doses to assess pathway-level enrichment and gene-expression patterns. Results: Several adjuvant combinations significantly increased antibody titers at 54 weeks compared with alum alone. Formulations containing cationic lipid or monophosphoryl lipid A (MPL) were associated with enhanced antibody responses. Early upregulation of immune-related genes across innate and adaptive pathways was also observed, with some combinations (e.g., inclusion of QS21 or ISCOMs) showing similar trends. Distinct group- and time-dependent transcriptional signatures were observed, with higher-responding formulations exhibiting stronger enrichment in pathogen-influenced signaling and cellular/humoral immune programs. Conclusions: Adjuvant selection and formulation strategy substantially modulate vaccine immunogenicity and early transcriptional programs, including innate, adaptive, and hematopoietic pathways. While individual adjuvants differentially regulate immune and platelet-associated genes, common pathway-level patterns emerge across formulations. These findings suggest candidate mechanisms for prolonged vaccine efficacy and provide actionable insights to guide rational adjuvant design for sustained immune protection.