About

Vincent K. Tsiagbe is an Associate Professor in the Department of Oral Biology at Rutgers School of Dental Medicine. His research over the past 30 years focuses on understanding the immunologic basis of B cell lymphoma development. He has unraveled a novel role for endogenous retroviruses in promoting germinal center-derived B cell lymphoma, demonstrating that endogenous retroviruses, which are gene segments of ancient infectious viruses integrated into the host genome, can be activated by lymphoma B cells to produce retroviral superantigens. These superantigens stimulate helper T cells to produce growth factors that support lymphoma B cell proliferation, a process he has termed “reverse immune surveillance.” His work includes cloning human endogenous retrovirus from human diffuse large B cell lymphoma (HERV-WL) and developing antibodies to detect cancer-associated antigens in aggressive cancers such as squamous cell carcinomas. Additionally, his research involves examining immunologic responses induced by the bacterium Actinobacillus actinomycetemcomitans during periodontal disease development, including the discovery of Bone Morphogenic Protein 10 (BMP10) production by lymphocytes and its role in lymphocyte activation.

Research topics

• Medicine
• Immunology
• Political Science
• Biology
• Sociology
• Cancer research
• Internal medicine
• Pathology
• Medical education
• Psychology
• Social psychology

Selected publications

• Intercellular Interaction Between a Dental Pulp Stem Cell and Leukemia Cells – Support of Acute Myeloid Leukemia

  International Journal of Translational Science · 2025-07-30

  articleOpen access

  The oral cavity is a site of hematopoietic activity, and metastatic hematological and solid tumors. This study focused on acute myeloid leukemia (AML) due to extensive documentation of its presentation in the gingiva. Despite these reports, it is unclear how AML and other leukemia cells survive in the oral tissue. We investigated intercellular communication between leukemia cells and dental pulp stem cells (DPSCs). DPSCs enhanced the proliferation and adhesion of AML cells (HL-60) and to a lesser extent, myelomoncytic leukemia cells (U937). The erythroleukemia K562 cells showed a delayed trend to proliferate. The communication between DPSCs and HL-60 cells was partly due to gap junctional intercellular communication (GJIC), as indicated by dye transfer. We also noted evidence of tunnelling nanotubules (TNT). Dye transfer was noted in non-adherent cells, suggesting other method of transfer, perhaps by extracellular vesicles. Using SORE-6 that can stratify the HL-60 subset, dye transfer occurred mostly in the subset lowest in the hierarchy. These latter findings were novel since they might provide insights into the behavior of non-leukemia stem cells and their interaction with cells in the oral cavity. In summary, this study began to dissect the interaction between HL-60 AML cells and DPSCs, providing insights into the survival of AML and perhaps other leukemia cells in the oral cavity.

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• Early Initiative of Structured Mentoring and Research for Social Disadvantage Trainees to Increase Diversity and Inclusion among Clinician Scientists

  Journal of Community Medicine & Public Health · 2024 · 2 citations

  • Sociology
  • Political Science
  • Medical education

  Background: There is a significant lag in integrating ethnically diverse healthcare trainees as clinician scientists. Although this gap is acknowledged, it is mostly focused physician scientists with a marked lag in dental scientists and the other healthcare fields such as the physician assistant program. We report on the outcome of three cohorts of underserved and economically disadvantaged trainees from a National Institute of Health Heart and Lung Blood Institute R25 summer training program with participants from four Rutgers Health Science schools. Objective: The goal was to support inclusivity within clinician scientist workforce through career development and education. Methods: We tested the hypothesis that early formal training with structured mentoring, research, career development, and didactic lectures will inspire trainees towards careers as clinician scientists. Trainees learned from the integration of research within the four health profession schools. We used a survey to assess how mentorship, research and career/educational development influence trainees' attitude for careers as clinician scientists. Career development included science communication, mentoring, data reproducibility, authorship, ethics in research, and models of healthcare institutional leadership. Results: >80% of the trainees continued their engagement in research with peer-reviewed publications, with confidence to engage in scientific discussion. Trainees developed a sense of belonging and a psychological safety net as they integrate with other groups of academic fields with confidence. Among 29 contacts, 87% responded. Less than 10% of incoming trainees indicated research in their career plans, which changed to >90% after one summer. Conclusions: Overall, this training program could serve as a `blueprint' for other programs to enhance careers in research, and to narrow the diversity gap among clinician scientists. Diversity among clinician scientists will enhance healthcare and disparities, and scientific innovation. Success would narrow the diversity gap among clinician scientists.

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• ELISA detection of human endogenous retroviral protein HERV-WL in saliva of cancer patients and normal individuals

  The Journal of Immunology · 2021

  1st authorCorresponding
  • Medicine
  • Biology
  • Internal medicine

  Abstract Previous studies revealed that a novel Human Endogenous Retrovirus (HERV-WL) was overexpressed in tissues from patients with certain aggressive human cancers, using immunohistochemistry techniques. ELISA detection also showed overexpression of HERV-WL in saliva of patients with certain aggressive cancers. To further explore these findings, saliva samples obtained from 12 patients with various cancers (1 with breast & colon cancer, 1, with colon cancer, 1 with multiple myeloma, 1 with prostrate cancer, 1 with renal carcinoma, and 7 with squamous cell carcinoma, were compared to saliva from 5 normal individuals. The studies showed significantly higher HERV-WL protein expression in saliva samples from all the 12 cancer patients (2–157 ug/ml), while HERV-WL protein expression was undetectable or less than 0.5 μg/ml in saliva from normal individuals. These findings warrant further research into the use of HERV-WL expression in saliva as a non-invasive assessment of responsiveness of certain cancers patients to therapy.

  PublisherDOI

• Dysbiosis From a Microbial and Host Perspective Relative to Oral Health and Disease

  Frontiers in Microbiology · 2021 · 78 citations

  • Biology
  • Immunology
  • Medicine

  The significance of microbiology and immunology with regard to caries and periodontal disease gained substantial clinical or research consideration in the mid 1960's. This enhanced emphasis related to several simple but elegant experiments illustrating the relevance of bacteria to oral infections. Since that point, the understanding of oral diseases has become increasingly sophisticated and many of the original hypotheses related to disease causality have either been abandoned or amplified. The COVID pandemic has reminded us of the importance of history relative to infectious diseases and in the words of Churchill "those who fail to learn from history are condemned to repeat it." This review is designed to present an overview of broad general directions of research over the last 60 years in oral microbiology and immunology, reviewing significant contributions, indicating emerging foci of interest, and proposing future directions based on technical advances and new understandings. Our goal is to review this rich history (standard microbiology and immunology) and point to potential directions in the future (omics) that can lead to a better understanding of disease. Over the years, research scientists have moved from a position of downplaying the role of bacteria in oral disease to one implicating bacteria as true pathogens that cause disease. More recently it has been proposed that bacteria form the ecological first line of defense against "foreign" invaders and also serve to train the immune system as an acquired host defensive stimulus. While early immunological research was focused on immunological exposure as a modulator of disease, the "hygiene hypothesis," and now the "old friends hypothesis" suggest that the immune response could be trained by bacteria for long-term health. Advanced "omics" technologies are currently being used to address changes that occur in the host and the microbiome in oral disease. The "omics" methodologies have shaped the detection of quantifiable biomarkers to define human physiology and pathologies. In summary, this review will emphasize the role that commensals and pathobionts play in their interaction with the immune status of the host, with a prediction that current "omic" technologies will allow researchers to better understand disease in the future.

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• Novel expression of Bone Morphogenic Protein 10 (BMP10) in lymphocytes

  The Journal of Immunology · 2019-05-01

  article1st authorCorresponding

  Abstract The bone morphogenic protein family (~20 BMPs in humans), are members of the transforming growth factor-β (TGF-β) superfamily. BMPs have been shown to exert important roles during development and organogenesis by delivering positional information in both vertebrates and invertebrates. We had previously observed early induction of mRNA for BMP10 in rat B cells soon after Aggregatibacter actinomycetemcomitans (Aa) bacterial infection, in studies conducted in a rat model for human periodontal disease. However, prior to the onset of bone resorption, BMP10 mRNA precipitously declined. Being the first demonstration that mRNA for BMP10 is expressed by lymphocytes, we examined the expression of BMP10, at the protein level. Peripheral blood lymphocytes from humans, rats and mice were purified, by micro-immunomagnetic bead separation, into B cell, CD4, and CD8 T cell fractions. Flow cytometry analysis conducted with anti-BMP10 antibody revealed cellular expression of BMP10 in all the fractions examined. Interestingly, activation of CD4 T cells by Con A, rodent B cells by LPS, or human B cells by S. Aureus, resulted in drastic shut-down of BMP10 expression at mRNA and protein levels. In conclusion, our studies demonstrate, for the first time, that lymphocytes express BMP10 protein. Furthermore, while activation of B cells by bacterial antigen induced early BMP10 expression, further chronic stimulation resulted in decline in BMP10 expression. Intriguingly, mitogen stimulation of B cells and CD4 T cells, led to a drastic reduction in BMP10 expression at mRNA and protein levels, suggesting that BMP10 might be a novel marker for naïve lymphocytes.

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• A Comparison of Aggregatibacter actinomycetemcomitans (Aa) Virulence Traits in a Rat Model for Periodontal Disease

  PLoS ONE · 2013-07-23 · 17 citations

  articleOpen access

  Our aim was to explore the effects of Cytolethal Distending toxin (Cdt) in a well established rat model of periodontal disease where leukotoxin (LtxA) was thought to have no known effect. In vitro studies, were used to assess CdtB activity using Aa Leukotoxin as a negative control. These studies showed that both CdtB and LtxA (unexpectedly) exerted significant effects on CD4(+) T cells. As a result we decided to compare the effects of these two prominent Aa virulence factors on bone loss using our rat model of Aa-induced periodontitis. In this model, Aa strains, mutant in cdtB and ltxA, were compared to their parent non-mutant strains and evaluated for colonization, antibody response to Aa, bone loss and disease. We found that bone loss/disease caused by the ltxA mutant strain, in which cdtB was expressed, was significantly less (p<0.05) than that due to the wild type strain. On the other hand, the disease caused by cdtB mutant strain, in which ltxA was expressed, was not significantly different from the wild type strain. This data indicates that Aa LtxA exerts a greater effect on bone loss than Cdt in this rat model of periodontal disease and supports the utility of this model to dissect specific virulence factors as they relate to immunopathology in studies of Aa-induced disease.

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• Aggregatibacter actinomycetemcomitans Infection Enhances Apoptosis <i>In Vivo</i> through a Caspase-3-Dependent Mechanism in Experimental Periodontitis

  Infection and Immunity · 2012-03-27 · 59 citations

  articleOpen access

  The purpose of this study was to test the hypothesis that diabetes aggravates periodontal destruction induced by Aggregatibacter actinomycetemcomitans infection. Thirty-eight diabetic and 33 normal rats were inoculated with A. actinomycetemcomitans and euthanized at baseline and at 4, 5, and 6 weeks after inoculation. Bone loss and the infiltration of polymorphonuclear leukocytes (PMNs) in gingival epithelium were measured in hematoxylin-eosin-stained sections. The induction of tumor necrosis factor alpha (TNF-α) was evaluated by immunohistochemistry and of apoptotic cells by a TUNEL (terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling) assay. After A. actinomycetemcomitans infection, the bone loss in diabetic rats was 1.7-fold and the PMN infiltration 1.6-fold higher than in normoglycemic rats (P < 0.05). The induction of TNF-α was 1.5-fold higher and of apoptotic cells was up to 3-fold higher in diabetic versus normoglycemic rats (P < 0.05). Treatment with a caspase-3 inhibitor significantly blocked noninflammatory cell apoptosis induced by A. actinomycetemcomitans infection in gingival epithelium and connective tissue (P < 0.05). These results provide new insight into how diabetes aggravates A. actinomycetemcomitans-induced periodontal destruction in rats by significantly increasing the inflammatory response, leading to increased bone loss and enhancing apoptosis of gingival epithelial and connective tissue cells through a caspase-3-dependent mechanism. Antibiotics had a more pronounced effect on many of these parameters in diabetic than in normoglycemic rats, suggesting a deficiency in the capacity of diabetic animals to resist infection.

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• <i>A.actinomycetemcomitans</i>‐induced periodontal disease promotes systemic and local responses in rat periodontium

  Journal Of Clinical Periodontology · 2012-02-07 · 19 citations

  article

  AIM: To characterize the histologic and cellular response to A. actinomycetemcomitans (Aa) infection. MATERIAL & METHODS: Wistar rats infected with Aa were evaluated for antibody response, oral Aa colonization, loss of attachment, PMN recruitment, TNF-α in the junctional epithelium and connective tissue, osteoclasts and adaptive immune response in local lymph nodes at baseline and 4, 5 or 6 weeks after infection. Some groups were given antibacterial treatment at 4 weeks. RESULTS: An antibody response against Aa occurred within 4 weeks of infection, and 78% of inoculated rats had detectable Aa in the oral cavity (p < 0.05). Aa infection significantly increased loss of attachment that was reversed by antibacterial treatment (p < 0.05). TNF-α expression in the junctional epithelium followed the same pattern. Aa stimulated high osteoclast formation and TNF-α expression in the connective tissue (p < 0.05). PMN recruitment significantly increased after Aa infection (p < 0.05). Aa also increased the number of CD8(+) T cells (p < 0.05), but not CD4(+) T cells or regulatory T cells (Tregs) (p > 0.05). CONCLUSION: Aa infection stimulated a local response that increased numbers of PMNs and TNF-α expression in the junctional epithelium and loss of attachment. Both TNF-α expression in JE and loss of attachment was reversed by antibiotic treatment. Aa infection also increased TNF-α in the connective tissue, osteoclast numbers and CD8(+) T cells in lymph nodes. The results link Aa infection with important characteristics of periodontal destruction.

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• CD30L null SJL mice exhibit reduced lymph node and spleen weights but support growth of transplantable SJL lymphoma RCS-X (48.29)

  The Journal of Immunology · 2011-04-01

  article1st authorCorresponding

  Abstract The process by which endogenous retroviral superantigen (vSAg29) expressing SJL lymphomas (RCS) stimulate host CD4+Vβ16+ T cells, in order to elicit help (notably IL-4 and -5) for their growth, has been characterized as “reverse immune surveillance”. This response is facilitated by the high expression of an array of co-stimulating molecules on RCS cells, including B7.1, B7.2, 41BBL, CD40 and CD30. On the basis of their germinal center derivation, SJL lymphomas bear close resemblance to a subpopulation of human germinal center B cell lymphomas, such as CD30+ Hodgkin’s lymphomas. In our earlier studies, growth of transplantable SJL lymphoma (RCS-X) in vivo was inhibited by anti-CD30 mAb. While the evidence shows that this effect is indirectly on the lymphoma-responsive CD4 T cells, the mechanism of action was unclear. To shed light on the role of CD30-CD30L interactions in SJL lymphoma development, CD30L-/- were bred onto SJL background and tested for their support of transplantable lymphoma growth. A significant reduction in lymph node (17.4-54.7%) and spleen weights (21.5-38.2%) was observed for CD30 null mice, compared to wild type SJL mice. Despite this reduction in the lymphoid compartment, no reduction in lymphoma growth was observed. The results suggest that while CD30-CD30L interactions might be important for SJL lymphoma growth, other costimulating molecules might contribute significantly to the process of reverse immune surveillance in RCS lymphoma.

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• Adaptive immune response in osteoclastic bone resorption induced by orally administered Aggregatibacter actinomycetemcomitans in a rat model of periodontal disease

  Molecular Oral Microbiology · 2010-07-05 · 53 citations

  articleSenior author

  There is mounting evidence that innate and adaptive immunity are critical for periodontal disease-mediated bone resorption. These studies examined the role of B and CD4 T cells in adaptive immunity of rats infected with Aggregatibacter actinomycetemcomitans (Aa). Sprague-Dawley male rats were fed Aa-containing mash or control-mash for 2 weeks. B and CD4 T cells were obtained from draining lymph nodes at 2, 4 and 12 weeks, postinoculation. Quantitative polymerase chain reaction-based messenger RNA expression was conducted for 89 cytokine family genes. Disease-relevance of the differentially expressed genes was assessed using a biological interaction pathway analysis software. B and CD4 T cells of Aa-infected rats increased and were activated, resulting in enhanced isotype-switched serum immunoglobulin G by 2 weeks postinoculation. Bone resorption was evident 12 weeks after Aa-feeding. In B cells, interleukin-2 (IL-2), macrophage-inhibiting factor, IL-19, IL-21, tumor necrosis factor (TNF), CD40 ligand (CD40L), CD70, bone morphogenetic protein 2 (BMP2), BMP3, and BMP10 were upregulated early; while IL-7, Fas ligand (FasL), small inducible cytokine subfamily E1, and growth differentiation factor 11 (GDF11; BMP11) were upregulated late (12 weeks). BMP10 was sustained throughout. In CD4 T cells, IL-10, IL-16, TNF, lymphotoxin-beta (LTbeta), APRIL, CD40L, FasL, RANKL and osteoprotegerin were upregulated early, whereas IL-1beta, IL-1RN, IL-1F8, IL-24, interferon-alpha1, GDF11 (BMP11), and GDF15 were upregulated late (12 weeks). Adaptive immunity appears crucial for bone resorption. Several of the deregulated genes are, for the first time, shown to be associated with bone resorption, and the results indicate that activated B cells produce BMP10. The study provides a rationale for a link between periodontal disease and other systemic diseases.

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Recent grants

• NIH Grant R01CA014462

  NIH · $5.0M · 2003

Frequent coauthors

• G. J. Thorbecke

  29 shared

• G. J. Thorbecke

  New York University

  29 shared

• Nicholas M. Ponzio

  17 shared

• Ross S. Basch

  NYU Langone Health

  9 shared

• Margaret Sunde

  University of Sydney

  9 shared

• Rajan M. Thomas

  Children's Hospital of Philadelphia

  8 shared

• J Asakawa

  Yamaguchi University

  8 shared

• W. J. Simmons

  8 shared