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Brice Gaudilliere

Brice Gaudilliere

· Associate Professor Of Anesthesiology, Perioperative And Pain Medicine (Adult-MSD) And, By Courtesy, Of Pediatrics (Neonatology)Verified

Stanford University · Rheumatology

Active 2002–2025

h-index39
Citations7.8k
Papers151100 last 5y
Funding$17.0M1 active
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About

Brice Gaudilliere is an Associate Professor of Anesthesiology, Perioperative and Pain Medicine at Stanford University, with a courtesy appointment in Pediatrics (Neonatology). He is affiliated with the Center for Artificial Intelligence in Medicine & Imaging (AIMI) at Stanford. His research focuses on the application of artificial intelligence and imaging techniques in medicine, particularly in the fields of anesthesiology, perioperative care, pain medicine, and neonatology. As a faculty member at Stanford, he contributes to advancing medical AI research and education, supporting initiatives that integrate AI technologies into healthcare practices.

Research topics

  • Medicine
  • Internal medicine
  • Biology
  • Pharmacology
  • Bioinformatics
  • Neuroscience
  • Pediatrics
  • Intensive care medicine
  • Immunology
  • Obstetrics
  • Psychiatry
  • Computational biology
  • Physiology
  • Genetics
  • Pathology

Selected publications

  • Supplementary Materials from Vγ9Vδ2 T Cells Express an Antitumor Profile Associated with Anti–PD-(L)1 Responses and Activation Defects Restored by Anti-BTN3A in Triple-Negative Breast Cancer

    2025-10-01

    articleOpen access

    <p>Supplementary Materials</p>

  • Systemic immune dysregulation in hypertensive disorders of pregnancy persists years after delivery

    bioRxiv (Cold Spring Harbor Laboratory) · 2025-11-29

    preprintOpen accessCorresponding

    Background: Hypertensive disorders of pregnancy (HDP), including preeclampsia and gestational hypertension, are associated with an increased risk of cardiovascular disease (CVD) later in life. Mechanisms that link HDP to CVD, however, remain unclear. Methods: We used a high-dimensional single-cell mass cytometry approach to profile the distribution and functional responses of maternal immune cells in three separate groups of HDP cases and normotensive controls, sampled antepartum, postpartum, and several years postpartum (midlife). We used multivariable sparse modeling to distinguish HDP cases from controls. Results: We accurately distinguished HDP cases from controls at all three study timepoints, with area under the receiver operator characteristic (AUROC) curve values of 0.814 for the antepartum group, 0.757 for the postpartum group, and 0.692 for the midlife group. Distinct immune signatures for each model underscore the dynamic dysregulation of the immune system throughout life. In addition, we identified a persistent immune dysregulation signal among HDP cases at all three timepoints, characterized by increased B cell frequency and decreased pSTAT3 response upon cytokine stimulation in classical monocytes. Conclusions: Persistent immune dysregulation among women with a history of an HDP may contribute to elevated long-term risk of CVD development.

  • Palmar cooling mitigates exercise-induced immune suppression after high-intensity training: A randomized trial

    medRxiv · 2025-11-07

    preprintOpen accessSenior authorCorresponding

    ABSTRACT Objectives We investigated whether palmar cooling alters inflammatory responses following a single session of high-intensity eccentric exercise. We hypothesized that palmar cooling during rest intervals would attenuate maladaptive inflammatory responses while preserving beneficial immune adaptations necessary for muscle repair and recovery. Methods In this randomized interventional study, 20 healthy adults were matched by sex and one-repetition maximum (1RM) for bicep curls. Participants performed 10 sets at 70% 1RM, receiving either palmar cooling at 14ºC or a thermoneutral control at 30ºC during 3-minute inter-set rest periods. Whole blood was collected at baseline, immediately post-exercise, and on post-exercise days 1, 2, and 4 for comprehensive immune profiling with mass cytometry. Blood lactate and pain scores were also recorded. Results Exercise induced broad immunosuppression that was significantly attenuated in the palmar cooling group by 2 days post-exercise (AUC=0.79, p =0.03). The cooled group had decreased immunosuppressive activity and increased inflammatory innate immune mechanisms in the cooled group. Palmar cooling also significantly reduced lactate levels compared to controls ( p =0.024). Conclusion Palmar cooling at 14ºC during rest intervals effectively modulated the immune response to high-intensity exercise and reduced lactate accumulation. These findings suggest palmar cooling may serve as a promising intervention to mitigate exercise-induced immunosuppression and support recovery. Trial identifier NCT07215338 (retrospectively registered). Summary Box What is already known on this topic High intensity eccentric exercise contributes to physiological heat stress which induces significant immune alterations that can lead to a transient period of immunosuppression and increased incidence of respiratory tract infections . What this study adds Palmar cooling resulted in cell-type-specific alterations in innate and adaptive immune cell signaling activity, particularly decreasing immunosuppressive cell responses while enhancing inflammatory innate immune mechanisms implicated in pathogen defense . How this study might affect research, practice or policy Palmar cooling may serve as an effective intervention for managing exercise-induced immunosuppression and supporting recovery in athletes. Integration of palmar cooling techniques into athletic training regimens and rehabilitation protocols can ultimately enhance exercise performance and reduce the adverse effects associated with high-intensity exercise .

  • Application of comprehensive multi-omic immune profiling strategy achieves superior checkpoint immunotherapy response prediction in lung cancer 3507

    The Journal of Immunology · 2025-11-01

    articleOpen access

    Abstract Description Immune checkpoint inhibitors (ICIs) are currently the most effective treatment for late-stage lung cancer. However, most patients fail to mount a durable response, and the mechanisms underlying non-responsiveness remain elusive. Here, we apply a universal omics approach to identify correlates of non-responsiveness to ICIs in lung cancer. In-depth characterization of the plasma proteome was performed using the SomaScan™ Platform on pretreatment and longitudinal blood samples from 40 ICI-treated patients, achieving quantification of 10,000 unique proteins. Comprehensive immune phenotyping was achieved with matched pretreatment PBMC for 90% of patients (36/40) through CyTOF™ technology, with a 38-plex panel describing over 150 immune populations in circulation. To enhance clinical outcome predictability of cellular and plasma-based immune relationships, cross-platform data integration was achieved with Stabl, a sparse, reliable omic biomarkers analysis strategy. Stabl identified key predictive features from both CyTOF and SomaScan technology, providing insight into immune deficits present in non-responsive patients. The combined model demonstrated a strong capability to predict non-response from a pretreatment blood sample (AUROC = 0.79, p-value = 1.7e-2, Mann-Whitney non-parametric test). Overall, robust treatment prediction, attributed to biomarker features, provides insights into mechanisms for non-response and highlights potential better treatment options in lung cancer. Funding Sources Supported by NHMRC Development Grant. Topic Categories Computational and Systems Immunology (COMP)

  • Table S13 from Vγ9Vδ2 T Cells Express an Antitumor Profile Associated with Anti–PD-(L)1 Responses and Activation Defects Restored by Anti-BTN3A in Triple-Negative Breast Cancer

    2025-10-01

    articleOpen access

    <p>LASSO analysis of Vg9Vd2 T cells outputs, related to Figure 5</p>

  • Guiding Parenteral Nutrition Therapy After Hematopoietic Stem Cell Transplantation

    Research Square · 2025-11-17

    preprintOpen access
  • Figure S8 from Vγ9Vδ2 T Cells Express an Antitumor Profile Associated with Anti–PD-(L)1 Responses and Activation Defects Restored by Anti-BTN3A in Triple-Negative Breast Cancer

    2025-10-01

    articleOpen access

    <p>Vg9Vd2 T cells display skewed differentiation profiles towards an early effector memory phenotype in untreated TNBC (related to Figure 3).</p>

  • Table S7 from Vγ9Vδ2 T Cells Express an Antitumor Profile Associated with Anti–PD-(L)1 Responses and Activation Defects Restored by Anti-BTN3A in Triple-Negative Breast Cancer

    2025-10-01

    articleOpen access

    <p>GSEA outputs based on the differentially expressed genes between Vg9Vd2 T cells versus abCD8 TemraTex, abCD8 Tem and Vd1 T cell in primary breast tumors, related to Figure 2</p>

  • Figure S6 from Vγ9Vδ2 T Cells Express an Antitumor Profile Associated with Anti–PD-(L)1 Responses and Activation Defects Restored by Anti-BTN3A in Triple-Negative Breast Cancer

    2025-10-01

    articleOpen access

    <p>Vg9Vd2 T cells are transcriptionally armed for type–I antitumor cytotoxic activity in untreated TNBC (related to Figure 2).</p>

  • Multiomic approach to study the immunologic profile preceding preterm birth

    Placenta · 2025-11-01

    article

Recent grants

Frequent coauthors

Education

  • MD

    Harvard Medical School

  • PhD

    Harvard University

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