About

Daniel Graves is an Assistant Professor in the Department of Economics at Harvard University. His primary fields of research are asset pricing, behavioral finance, and household finance. Graves's research focuses on studying the attention, beliefs, and information of institutional investors and households. He received his Ph.D. from Yale University in 2025, and he previously earned a simultaneous BA/MA from Yale.

Research topics

• Medicine
• Immunology
• Endocrinology
• Internal medicine
• Cell biology
• Biology
• Pathology
• Microbiology
• Cancer research
• Surgery
• Genetics

Selected publications

• LB1264 Treatment of murine atopic dermatitis with a CCL11 antibody and a topical CCR3 inhibitor

  Journal of Investigative Dermatology · 2025-07-21

  articleOpen access
  PublisherOA PDFDOI

• Diabetes exacerbates destructive inflammation by activating the CD137L-CD137 axis in dendritic and IL-17+ T cells

  Journal of Clinical Investigation · 2025-12-11

  articleOpen accessSenior author

  Periodontal disease, a bacterial infection affecting a large percentage of the world's population, is an important risk factor for several systemic diseases and is significantly worsened by diabetes. To investigate how diabetes exacerbates the inflammatory response to bacteria in this disease, we combined insights from murine and human studies. Through single-cell RNA-Seq, we identified a compelling hyperglycemia-driven molecular pathway: the upregulation of CD137L in dendritic cells (DCs) and increased expression of its receptor, CD137, in IL-17+ T cells. The CD137L-CD137 axis emerged as a pivotal mediator of diabetes-induced inflammatory tissue destruction. Antibody-mediated inhibition of CD137L markedly reduced diabetes-driven bone loss, neutrophil recruitment, expansion of γδ T cells, and excessive infiltration by IL-17A+ cells. In vitro studies further validated these findings and established that dysregulation of DCs mediated by high glucose levels dramatically altered γδ T cell activity in co-culture systems via CD137L. The essential role of DCs as CD137L producers in vivo was definitively established through lineage-specific Akt1 deletion, which abrogated CD137L expression in DCs and reversed the adverse effects of hyperglycemia on increased IL-17+ T cells and loss of Tregs in vivo. Conversely, activation of CD137 with an agonist in normal animals recapitulated diabetes-induced abnormalities in the inflammatory response and accelerated bone loss. These findings elucidate a key mechanism underlying diabetes-induced immune dysregulation and inflammatory damage, and point to the CD137L-CD137 pathway as a promising therapeutic target, offering potential insights into mitigating other diabetes-associated complications linked to inflammatory changes.

  PublisherOA PDFDOI

• Comparison of the bone remodeling in the midpalatal suture during maxillary expansion between young and middle-aged mice

  Bone · 2025-05-03

  articleOpen accessSenior author
  PublisherOA PDFDOI

• Understanding the Periodontitis–Diabetes Linkage: Mechanisms and Evidence

  Journal of Dental Research · 2025-11-25 · 5 citations

  articleOpen access1st authorCorresponding

  Diabetes mellitus (DM) and periodontitis share a complex, bidirectional relationship, with each condition exacerbating the other. Diabetes, particularly when poorly controlled, significantly increases the risk, severity, and progression of periodontitis. The biological mechanisms involved are complex and numerous. Hyperglycemia in diabetes is linked to oral microbial dysbiosis, which is in turn associated with increased inflammation, epithelial barrier dysfunction, impaired neutrophil and macrophage function, altered T-cell profiles, and cytokine imbalance, collectively fostering chronic inflammation and immune dysregulation. Moreover, diabetes alters bone metabolism, promoting osteoclastogenesis and reducing reparative bone regeneration by limiting coupled bone formation through an effect on growth factor production, mesenchymal stems cells, and osteoblasts. Conversely, periodontitis is strongly linked to poor glycemic control. Clinical studies and longitudinal meta-analyses report consistent positive associations, while randomized controlled trials show that periodontal therapy reduces HbA1c by ~0.43%. Emerging evidence suggests that periodontitis and oral preclinical dysbiosis contribute to diabetogenesis, although causality remains uncertain. Periodontitis may drive metabolic dysfunction through several biological mechanisms. The dysbiotic oral microbiome and subsequent periodontitis may promote systemic inflammation and subsequent insulin resistance and glucose intolerance. Moreover, oral dysbiosis may deplete nitrate-reducing taxa and impair nitric oxide pathways, which has relevance to both periodontal and cardiometabolic health. Accordingly, periodontal treatment in diabetic populations has shown potential health care savings. Nevertheless, trials assessing the influence of periodontitis treatment on systemic outcomes consistently show significant treatment heterogeneity, which requires explication in future studies. This review underscores the systemic implications of periodontitis in diabetes and highlights the value of integrating periodontal care into diabetes management. A better understanding of the shared pathophysiology between these diseases supports interdisciplinary approaches and points toward novel preventive and therapeutic strategies targeting inflammation, microbial balance, and host response modulation to jointly benefit periodontal and cardiometabolic health.

  PublisherDOI

• Single Cell Sequencing Identifies Distinct Cellular Alterations in Impaired Aged and Diabetic Wounds

  Aging Cell · 2025-11-04 · 2 citations

  articleOpen accessSenior authorCorresponding

  Impaired wound healing in aged and diabetic wounds involves complex cellular dysregulation that hinders tissue repair. Using single-cell RNA sequencing (scRNA-seq) and validation techniques, we investigated impaired wound healing to identify whether there were significant changes linked to each condition. Comparative mucosal wound analysis revealed distinct differences between diabetic and normoglycemic (NG)-aged mice, which had an impact on connective tissue formation and epithelial closure. Wounds in NG-aged mice exhibited prolonged granulation tissue and upregulation of genes linked to chemotaxis, cell migration, neutrophil degranulation, and antimicrobial defense pathways compared to the diabetic wounds. In comparison to healing in young animals, wounds in NG-aged mice had a shift in fibroblast subtypes with fewer matrix-producing myofibroblasts and increased inflammatory fibroblasts. Furthermore, wounds in NG-aged mice versus wounds in diabetic mice had an upregulation of lytic enzymes, with striking differences in cathepsin-expressing fibroblasts. Since diabetic wounds healed more slowly than wounds in NG-aged mice, the results suggest that the upregulation of lytic enzymes that characterized diabetic wounds is particularly damaging to healing. In addition to the transcriptional differences, pseudotime analysis revealed that fibroblasts in wounds from diabetic mice progressed towards a protease-enriched state, while those in aged mice shifted towards an inflammatory phenotype. This is the first study to directly compare aged and diabetic healing at the single-cell level and provides distinct molecular mechanisms that may allow more precise therapeutic targets to improve healing in aged and diabetic wounds.

  PublisherOA PDFDOI

• Single-cell RNA profiling identifies immune cell population shifts in diabetes associated mucosal inflammation

  Mucosal Immunology · 2025-07-02 · 4 citations

  articleOpen accessSenior author
  PublisherOA PDFDOI

• Sustained Release of Salicylic Acid for Halting Peri-Implantitis Progression in Healthy and Hyperglycemic Systemic Conditions: A Gottingen Minipig Model

  ACS Biomaterials Science & Engineering · 2024-04-09 · 6 citations

  articleOpen access

  To develop a peri-implantitis model in a Gottingen minipig and evaluate the effect of local application of salicylic acid poly(anhydride-ester) (SAPAE) on peri-implantitis progression in healthy, metabolic syndrome (MS), and type-2 diabetes mellitus (T2DM) subjects. Eighteen animals were allocated to three groups: (i) control, (ii) MS (diet for obesity induction), and (iii) T2DM (diet plus streptozotocin for T2DM induction). Maxillary and mandible premolars and first molar were extracted. After 3 months of healing, four implants per side were placed in both jaws of each animal. After 2 months, peri-implantitis was induced by plaque formation using silk ligatures. SAPAE polymer was mixed with mineral oil (3.75 mg/μL) and topically applied biweekly for up to 60 days to halt peri-implantitis progression. Periodontal probing was used to assess pocket depth over time, followed by histomorphologic analysis of harvested samples. The adopted protocol resulted in the onset of peri-implantitis, with healthy minipigs taking twice as long to reach the same level of probing depth relative to MS and T2DM subjects (∼3.0 mm), irrespective of jaw. In a qualitative analysis, SAPAE therapy revealed decreased levels of inflammation in the normoglycemic, MS, and T2DM groups. SAPAE application around implants significantly reduced the progression of peri-implantitis after ∼15 days of therapy, with ∼30% lower probing depth for all systemic conditions and similar rates of probing depth increase per week between the control and SAPAE groups. MS and T2DM conditions presented a faster progression of the peri-implant pocket depth. SAPAE treatment reduced peri-implantitis progression in healthy, MS, and T2DM groups.

  PublisherOA PDFDOI

• Advanced Imaging in Dental Research: From Gene Mapping to AI Global Data

  Journal of Dental Research · 2024-10-27 · 3 citations

  editorialOpen access1st author

  Advances in imaging technologies combined with artificial intelligence (AI) are transforming dental, oral, and craniofacial research. This editorial highlights breakthroughs ranging from gene expression mapping to visualizing the availability of global AI data, providing new insights into biological complexity and clinical applications.

  PublisherOA PDFDOI

• <scp>FOXO1</scp> regulates wound‐healing responses in human gingival fibroblasts

  Journal of Periodontal Research · 2024-03-18 · 3 citations

  articleOpen access

  BACKGROUND AND OBJECTIVE: Forkhead box-O 1 (FOXO1) is a transcription factor actively involved in oral wound healing at the epithelial barrier. However, less is known regarding the role of FOXO1 during the tissue repair response in the connective tissue compartment. This study explored the involvement of FOXO1 in the modulation of fibroblast activity related to wound healing. METHODS: Primary cultures of human gingival fibroblasts were obtained from four healthy young donors. Myofibroblastic differentiation, collagen gel contraction, cell migration, cell spreading, and integrin activation were evaluated in the presence or absence of a FOXO1 inhibitor (AS1842856). Variations in mRNA and proteins of interest were evaluated through qRT-PCR and western blot, respectively. Distribution of actin, α-smooth muscle actin, and β1 integrin was evaluated using immunofluorescence. FOXO1 and TGF-β1 expression in gingival wound healing was assessed by immunohistochemistry in gingival wounds performed in C57BL/6 mice. Images were analyzed using ImageJ/Fiji. ANOVA or Kruskal-Wallis test followed by Tukey's or Dunn's post-hoc test was performed. All data are expressed as mean ± SD. p < .05 was considered statistically significant. RESULTS: FOXO1 inhibition caused a decrease in the expression of the myofibroblastic marker α-SMA along with a reduction in fibronectin, type I collagen, TGF-β1, and β1 integrin mRNA level. The FOXO1 inhibitor also caused decreases in cell migration, cell spreading, collagen gel contraction, and β1 integrin activation. FOXO1 and TGF-β1 were prominently expressed in gingival wounds in fibroblastic cells located at the wound bed. CONCLUSION: The present study indicates that FOXO1 plays an important role in the modulation of several wound-healing functions in gingival fibroblast. Moreover, our findings reveal an important regulatory role for FOXO1 on the differentiation of gingival myofibroblasts, the regulation of cell migration, and collagen contraction, all these functions being critical during tissue repair and fibrosis.

  PublisherOA PDFDOI

• An update on periodontal inflammation and bone loss

  Frontiers in Immunology · 2024-06-11 · 60 citations

  reviewOpen accessSenior authorCorresponding

  Periodontal disease is a chronic inflammatory condition that affects the supporting structures of the teeth, including the periodontal ligament and alveolar bone. Periodontal disease is due to an immune response that stimulates gingivitis and periodontitis, and its systemic consequences. This immune response is triggered by bacteria and may be modulated by environmental conditions such as smoking or systemic disease. Recent advances in single cell RNA-seq (scRNA-seq) and in vivo animal studies have provided new insight into the immune response triggered by bacteria that causes periodontitis and gingivitis. Dysbiosis, which constitutes a change in the bacterial composition of the microbiome, is a key factor in the initiation and progression of periodontitis. The host immune response to dysbiosis involves the activation of various cell types, including keratinocytes, stromal cells, neutrophils, monocytes/macrophages, dendritic cells and several lymphocyte subsets, which release pro-inflammatory cytokines and chemokines. Periodontal disease has been implicated in contributing to the pathogenesis of several systemic conditions, including diabetes, rheumatoid arthritis, cardiovascular disease and Alzheimer’s disease. Understanding the complex interplay between the oral microbiome and the host immune response is critical for the development of new therapeutic strategies for the prevention and treatment of periodontitis and its systemic consequences.

  PublisherOA PDFDOI

Recent grants

• NIH Grant R03DE007556

  NIH · $21k · 1987

• Diabetes reversal and the subgingival microbiota

  NIH · $2.4M · 2018–2025

• Dendritic Cells and Periodontal Disease

  NIH · $4.2M · 2012–2025

• Mechanisms for Impaired Diabetic Wound Healing

  NIH · $4.8M · 2026–2031

• NIH Grant R23DE007559

  NIH · $130k · 1988

Frequent coauthors

• L. C. Gerstenfeld

  Boston University

  69 shared

• Elise F. Morgan

  Boston University

  53 shared

• Yanling Jiang

  South China Agricultural University

  52 shared

• Nathan A. Wigner

  University of Pennsylvania

  51 shared

• Manish V. Bais

  Boston University

  50 shared

• R. Toholka

  Boston University

  50 shared

• Alain Guignandon

  Université Jean Monnet

  49 shared

• Stefano Zanotti

  49 shared

Education

• Ph.D., Economics

  Harvard University

  2000

• B.A., Economics

  Harvard University

  1995