About

Laura Vella, M.D., Ph.D., is an Assistant Professor of Pediatrics (Infectious Diseases) at the University of Pennsylvania's Perelman School of Medicine. She is affiliated with the Department of Pediatrics and has graduate group affiliations in Immunology. Her educational background includes a BA in Biology with a Minor in English from the University of Delaware, a PhD in Immunology from the University of Pittsburgh School of Medicine, and an MD from the University of Pittsburgh School of Medicine. She completed her training in 2008 and 2010 respectively, and joined the University of Pennsylvania in 2019. Her research focuses on immunology, with significant contributions to understanding immune responses in various contexts, including infectious diseases and vaccine responses. She has co-authored studies on germinal center CD4 T follicular helper cells, immune dynamics in healthy adults, and immune predictors of vaccine readiness in patients with lymphoma and CLL. Her work involves multi-omic profiling and single-cell analysis to elucidate age-related immune reprogramming and immune cell heterogeneity. Dr. Vella's research aims to advance knowledge of immune mechanisms and improve clinical interventions in infectious diseases and immunology.

Research topics

• Immunology
• Medicine
• Virology
• Biology
• Pathology
• Internal medicine
• Computer Science
• Genetics
• Computational biology

Selected publications

• Author Correction: Multi-omic profiling reveals age-related immune dynamics in healthy adults

  Nature · 2026-04-10

  articleOpen access
  PublisherOA PDFDOI

• Macrophage Activation Syndrome–Associated Proteins and Enhanced Interferon‐γ Responsiveness in the Plasma Proteome of Patients With Multisystem Inflammatory Syndrome in Children in a Pretreatment Replication Single‐Center Cohort

  ACR Open Rheumatology · 2026-02-01

  articleOpen access

  OBJECTIVE: Multisystem inflammatory syndrome in children (MIS-C) is a rare hyperinflammatory syndrome that follows SARS-CoV-2 infection. Prior plasma proteomic analysis from a 2020 cohort of patients with MIS-C at our center revealed a profile characterized by thrombotic microangiopathy (TMA), macrophage activation syndrome (MAS)-associated proteins, and dysregulated interferon-γ (IFNγ) responses. However, a limitation of that study was that samples were often acquired after treatment. The objective of this study was to identify plasma proteomic signatures that uniquely define MIS-C versus other viral syndromes unconfounded by treatment effects in an independent cohort. METHODS: Plasma proteomics was performed using the Olink Explore HT platform on plasma from patients enrolled at emergency department admission with suspected MIS-C (final diagnoses N = 12 MIS-C, N = 30 other viral syndromes). Plasma autoantibody analysis was performed using a custom microbead-based protein array. RESULTS: Consistent with findings in the 2020 cohort, TMA- and MAS-associated proteins were more highly expressed, and there was a higher CXCL9 response to IFNγ in MIS-C compared to viral infection. In contrast to the 2020 cohort, patients with MIS-C did not have lower expression of the IFNγ suppressive protein TRIM21. On reanalysis of the 2020 cohort, only patients who received intravenous Ig (IVIg) treatment before sampling had low TRIM21 (also known as Ro52/SSA). IVIg recipients also had anti-Ro52 autoantibodies. CONCLUSION: We have validated several unique features of the plasma proteome of patients with MIS-C first identified in 2020. Discrepant TRIM21 expression in these two cohorts is due to anti-Ro52 autoantibodies in IVIg-treated patients. These data support the use of plasma cytokine profiling to rapidly diagnose MIS-C.

  PublisherDOI

• Rapid immune reconstitution in patients with transfusion-dependent thalassemia following betibeglogene autotemcel: A real-world experience

  Blood · 2025-11-03

  articleOpen access

  Abstract Introduction: Gene therapies for transfusion-dependent thalassemia (TDT) such as betibeglogene autotemcel (beti-cel) alleviate transfusion dependence. These therapies use single-agent busulfan myeloablative conditioning (Bu-MAC) and CD34+ selected autologous gene-modified hematopoietic stem cells (GM-HSCs) depleted of T cells. Bu-MAC is less immunosuppressive compared to conventional allogeneic HSC transplant (allo-HSCT) conditioning; however, the combined impact of Bu-MAC and CD34+ selection on immune reconstitution is not known. Therefore, most centers use infection surveillance/prophylaxis and revaccination protocols developed for allo-HSCT. These protocols isolate patients for months and incur costs and potential toxicities. Yet, prolonged caution may be unnecessary; pre-clinical animal models and a clinical study of autologous transplant suggest that Bu-MAC may only transiently reduce absolute lymphocyte counts (ALCs). Therefore, we hypothesized that patients with TDT reconstitute immune function sooner after beti-cel than after allo-HSCT. Methods: We conducted a single-center retrospective cohort study of children and young adults with TDT who received beti-cel post-FDA approval at the Children's Hospital of Philadelphia (CHOP) and consented to the CHOP Bone Marrow Transplant Biorepository. Results reported from the time of beti-cel infusion. Cell counts reported as median and range cells/μL. ALCs were assessed frequently before and after infusion. Clinical lymphocyte subsets, PHA-induced T cell proliferation, immunoglobulin concentrations, and tetanus titers were measured before and at 3-month intervals after infusion or until vaccination thresholds were met. Vaccination thresholds were defined per the CHOP transplant section standard of care: absolute CD4+ T cells ≥ 200 cells/μL, T cell PHA stimulation ≥ 30% of control, IgG > 400 mg/dL (and ≥3 months from IVIG infusion), and evidence of IgA or IgM recovery or presence of switched memory B cells. Tetanus titers considered protective if ≥ 0.1 IU/mL. For deep immune cell profiling, we analyzed Ficoll-separated peripheral blood mononuclear cells from a subset of these patients collected 2-, 6-, and 8-months post infusion with a 31-color spectral flow cytometry panel. Circulating T follicular helper cells (cTfh) reported as percent of non-naïve CD4+ T cells that are CXCR5+. Results: We identified 9 patients eligible for the cohort. None had undergone prior splenectomy. Median ALC nadir was 500 (range: 390-1370) and occurred after approximately 2 weeks. Median primary lymphocyte subset counts recovered to and persisted at or above near-normal levels for age for all patients by 3 months: CD3+ = 893 (438-1856), CD3+, CD4+ = 415 (206-675), CD3+, CD8+ = 485 (178-1157), CD19+ = 287 (120-655), NK cells = 104 (47-348). All patients' T cell PHA stimulation responses and immunoglobulin levels met vaccination thresholds at all timepoints. By 3 months, 8 of 9 patients had near-normal counts of naïve (CD19+, IgD+, CD27-) and unswitched memory (CD19+, IgD+, CD27+) B cells – both associated with generating durable protective vaccine responses. 8 of 9 patients also had protective tetanus titers prior to and retained after infusion, including before revaccination. All samples analyzed by spectral flow cytometry contained near-normal percentages for age of all primary lymphocyte subsets. cTfh, critical for generating durable protective vaccine responses, were present throughout: median: 14.1%, (5.46-24.0%). Conclusions: These findings suggest that patients with TDT treated with beti-cel are functionally lymphocyte replete 3 months after Bu-MAC and infusion of CD34+ selected GM-HSCs and remain so thereafter. Three months after infusion, patients possessed sufficient lymphocyte subset counts and PHA-induced T cell proliferation responses suggesting that patients may not require further monitoring or prophylaxis for viral reactivation. Patients also had B and T cell subsets associated with generating protective vaccine responses signaling potential vaccine-readiness at this time. Furthermore, immunoglobulins and protective tetanus titers persisted independent of IVIG suggesting that plasma cell function may be unaffected by Bu-MAC. Together these findings suggest that patients with TDT likely retain protective vaccine titers, which combined with adequate lymphocyte function, may not require prolonged isolation or full revaccination post-GM-HSCT in contrast to patients post-allo-HSCT.

  PublisherOA PDFDOI

• Longitudinal multi-omic immune profiling of the healthy pediatric immune system and its response to vaccination 3300

  The Journal of Immunology · 2025-11-01

  articleOpen access

  Abstract Description Investigations of human immune responses typically focus on adults, resulting in limited knowledge of the pediatric immune system and how it responds to distinct challenges early in life. To bridge this gap, we conducted a 3-year longitudinal multi-omic profiling study of 46 healthy children aged 11-13 as they received flu, HPV, DTaP, and COVID vaccines. This dataset includes scRNAseq of > 3.5 million PBMCs classified into 70 immune cell types based on our Immune Health Atlas, as well as plasma proteomics and high-dimensional flow cytometry. We are utilizing this dataset to characterize the pediatric immune system at baseline and in response to acute and chronic challenges as it compares to the adult immune system, with the ability to compare neoantigen and recall responses within the same children. This analysis revealed age-independent and age-dependent response patterns, with similar cellular compositions and gene-expression changes characterizing response to chronic CMV infection between children and adults but heightened activity in specific cell types responding to flu vaccination in children. We also identified increased activity in specific cell types in response to vaccines that elicit recall as opposed to neoantigen responses, providing a means to understand how immune memory is established and re-engaged in children. These initial findings lay the groundwork upon which we can build and deepen our understanding of immune dynamics in early adolescence. Topic Categories Vaccines and Immunotherapy (VAC)

  PublisherOA PDFDOI

• Dysregulated lymphocyte localization in idiopathic multicentric Castleman disease

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-12-15 · 1 citations

  articleOpen access

  Idiopathic multicentric Castleman disease (iMCD) is a rare and life-threatening hematologic disease involving episodic flares of uncontrollable systemic inflammation by unknown causes. Hallmark features of iMCD include multiple enlarged lymph nodes with characteristic histopathological phenotypes and a potentially fatal, cytokine release syndrome. The key pathophysiologic drivers of disease are poorly understood and few effective treatment options exist. Here, we discovered an association between elevated chemokines, namely CXCL13, and lymph node size in iMCD, providing one possible explanation for the lymphadenopathy observed clinically. Instead of a concurrent increase in circulating CXCL13 and CXCR5-expressing cells that has been described in other contexts, during active disease, chemokine-responsive lymphocytes downregulated CXCR5 levels in iMCD. Despite heightened chemokine production by lymph node stromal cells, T and B cells failed to appropriately respond to their cues locally within the tissue and were particularly scarce within CXCL13-expressing germinal centers (GC). Inflammatory signals in iMCD lymph nodes appeared to restrict the production and movement of T follicular helper cells, which play an important role in facilitating appropriate GC responses. Together, these data provide a link between dysregulated chemokine production and germinal center lymphocyte trafficking, highlighting a potential mechanism and therapeutic target in iMCD lymphadenopathy. One Sentence Summary: Lymphocyte chemotaxis to discrete areas of lymphoid tissue is disrupted in idiopathic multicentric Castleman disease.

  PublisherOA PDFDOI

• P-637. Infection Incidence and Trajectory of Immune Recovery in Children, Adolescents, and Young Adults After Chemotherapy for Acute Lymphoblastic Leukemia

  Open Forum Infectious Diseases · 2025-01-29 · 1 citations

  articleOpen access

  Abstract Background Advances in chemotherapy for acute lymphoblastic leukemia (ALL) have improved survival rates, but survivors remain vulnerable to infection after completing chemotherapy. Data have shown increased infection risk for pediatric ALL survivors compared to healthy children, yet few studies have prospectively tracked infection rates alongside immune recovery. This study aims to quantify infection incidence and describe the trajectory of immune reconstitution in the year after ALL therapy completion. Methods Patients aged 3-30 completing ALL therapy at a pediatric center are being followed for the first year off-therapy. Total immunoglobulin-G (IgG) and antibody (Ab)-specific IgG levels for varicella, measles, and 23 pneumococcal serotypes are measured at 3, 6, and 12 months. Infection events are recorded monthly to calculate infection incidence per 1000 patient-days. Results To date, 21 patients have been followed for ≥ 6 months. Median age at ALL diagnosis was 7.3 years (IQR: 3.4-10.1). 67% of patients had ≥ 1 infections; 93% of those with infections had ≥ 2. The overall infection incidence rate was 6.1 per 1000 patient-days. Of 46 infections, upper respiratory illness (20, 43.5%) and gastroenteritis (6, 13%) were most common (Table 1). 17 of 21 patients had not received intravenous immunoglobulin replacement (IVIG) within 6 months of therapy completion; their mean total IgG was 859.6 mg/dL at 3 months and 918.2 mg/dL at 6 months (Table 2). All 17 received ≥ 1 pneumococcus, varicella, and/or measles vaccine before ALL diagnosis. None had evidence of pneumococcus or varicella Ab recovery at 6 months, regardless of pre-ALL partial or full vaccination status (Tables 2-3). 7/11 patients fully vaccinated and 3/6 partially vaccinated for measles before diagnosis had normal Ab indices at 6 months off-therapy (Table 4). Conclusion Infections were common during the first year off-therapy, with many experiencing multiple illnesses. Total IgG levels were reasonable at 3 and 6 months, but there was no recovery of varicella or pneumococcus Ab, and only a subset of patients retained measles Ab. Continued assessment until 12-month follow-up for all 85 enrolled patients is necessary but preliminary data suggest potential need for Ab-informed revaccination. Disclosures Brian T. Fisher, DO, MPH/MSCE, Allovir: Grant/Research Support|Astellas: Data Safety Monitoring Board|Merck: Grant/Research Support|Pfizer: Grant/Research Support

  PublisherOA PDFDOI

• Multimodal analysis defines <i>GNG4</i> as a distinguishing feature of germinal center-positioned CD4 T follicular helper cells in humans

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-12-13 · 1 citations

  preprintOpen accessSenior authorCorresponding

  Abstract CD4 T follicular helper (Tfh) cells coordinate humoral immune responses within germinal centers (GC) of lymphoid tissue. Despite their critical roles in vaccination and autoimmunity, the gene expression programs that define functionally distinct human Tfh states— and the molecular pathways engaged by Tfh positioned within the GC niche—remain incompletely understood. This gap has limited translational efforts to monitor or therapeutically target specific Tfh states for clinical benefit. Here, we delineate human CD4 T cell heterogeneity in tonsils and peripheral blood using trimodal single-cell sequencing and spectral flow cytometry to define epigenomic, transcriptional, and proteomic features of distinct Tfh states. Tfh with a GC-like phenotype exhibited markedly increased chromatin accessibility and both mRNA and protein expression of G protein subunit gamma 4 ( GNG4) . In tonsil, single-cell spatial transcriptomics defined GNG4 expression as a distinguishing feature of activated Tfh states within spatially demarcated GC compartments, with greater specificity than conventionally GC-associated features such as BCL6, TOX2, and S1PR2 . In contrast, GNG4 − Tfh primarily localized to nonGC regions and exhibited a resting, Th17-polarized phenotype. Together, these data highlight GNG4 as a central feature of activated, GC-positioned Tfh cell identity in humans. One Sentence Summary GNG4 expression defines activated CD4 T follicular helper cells localized to the germinal center of human lymphoid tissue.

  PublisherDOI

• Multi-omic profiling reveals age-related immune dynamics in healthy adults

  Nature · 2025-10-29 · 33 citations

  articleOpen access

  The generation and maintenance of immunity is a dynamic process that is dependent on age1–3. Here, to better understand its progression, we profiled peripheral immunity in more than 300 healthy adults (25 to 90 years of age) using single-cell RNA sequencing, proteomics and flow cytometry, following 96 adults longitudinally across 2 years with seasonal influenza vaccination. The resulting resource generated a single-cell RNA-sequencing dataset of more than 16 million peripheral blood mononuclear cells with 71 immune cell subsets from our Human Immune Health Atlas and enabled us to interrogate how immune cell composition and states shift with age, chronic viral infection and vaccination. From these data, we demonstrate robust, non-linear transcriptional reprogramming in T cell subsets with age that is not driven by systemic inflammation or chronic cytomegalovirus infection. This age-related reprogramming led to a functional T helper 2 (TH2) cell bias in memory T cells that is linked to dysregulated B cell responses against highly boosted antigens in influenza vaccines. Collectively, this study reveals unique features of the immune ageing process that occur prior to advanced age and provides novel targets for age-related immune modulation. We provide interactive tools for exploring this extensive human immune health resource at https://apps.allenimmunology.org/aifi/insights/dynamics-imm-health-age/ . This multi-omic longitudinal analysis of the healthy human peripheral immune system constructs the Human Immune Health Atlas and assembles data on immune cell composition and state changes with age, including responses to cytomegalovirus infection and influenza vaccination.

  PublisherOA PDFDOI

• Cellular features of graft vs host disease prophylaxis impact on CD4 T cell reconstitution post allo-HCT

  Blood · 2025-11-03

  articleSenior author

  Abstract Introduction: Immune reconstitution after allogeneic hematopoietic cell transplantation (allo-HCT) is required for protection from infection and response to vaccination. The phase 3 BMT-CTN 1703 trial comparing Graft versus Host Disease (GVHD) prophylaxis regimens suggested that post-transplant cyclophosphamide (PTCy) significantly improved GVHD-free relapsed-free survival without a significant impact on overall survival. Its companion study (BMT CTN 1801) showed that PTCy resulted in an early reduction of T-Cell Receptor (TCR) repertoire diversity that persisted for at least 2 years. However, this important finding was observed amongst total CD3+ T cells. We therefore asked whether the restricted clonality and clonal behavior of T cells over time was driven by reduced naive cell frequency or whether clonality defects were intrinsic to the transplant protocol and persisted into CD4 T cells after antigen exposure. Method: To capture features of the emerging immune systems between conventional GVHD prophylaxis regimens (Tac/MTX or Tac/MMF) used after matched unrelated donor (MUD) transplant versus tacrolimus with post-transplant cyclophosphamide (Tac/PTCy) used as GVHD prophylaxis after haploidentical HCT, we performed deep immunophenotyping on a cohort of 10 adults who received allo-HCT from peripheral blood stem cells (PBSCs). Of the 10 individuals, 6 received Tac/MTX or Tac/MMF and 4 received Tac/PTCy. Acute and chronic GVHD were diagnosed in 6 of 10 individuals, distributed across both conventional and PTCy prophylaxis groups. Peripheral blood mononuclear cells (PBMCs) were drawn at 1, 2, 3, 6, and 12 months post-transplant. PBMCs from 8 age-approximated healthy individuals were included as normal immune controls. PBMCs were analyzed with a high-parameter panel on a Cytek spectral flow cytometer, and viable lymphocytes were sorted for downstream 10x 5' scRNA-seq and immunoreceptor sequencing. Result: Broad measures of immune reconstitution in our analysis recapitulated prior studies, suggesting that PTCy is associated with early and sustained reduction of naive CD4 T cells through 1yr post-transplant as well as reduced clonal diversity assessed in both single cell and bulk TCR sequencing (TCRseq). Instead of naive cells, individuals who received haplo/PTCy HCT were more likely to expand effector memory CD4 T cells. Due to the single cell nature of our data, we were able to ask if the reduced clonal diversity observed after PTCy might be driven solely by a loss of naive CD4 T cells, which are the least clonally expanded and most clonally diverse T cell population in blood. In the analysis of non-naive CD4 T cells, our scTCRseq data indicate similar TCR diversity in haplo/PTCy and MUD/MTX HCT recipients once cells encounter antigen. We next used the single cell resolution in our data to understand whether clonal plasticity – the ability of a clone to be found across multiple CD4 T cell phenotypes – was observed after transplant and if differences exist between haplo/PTCy vs MUD/conventional prophylaxis. We performed clonal plasticity analysis of the top 50 clones per person across all timepoints. We observed significantly higher clonal plasticity rates in haplo/PTCy recipients. The most plastic clones were observed as a dynamic transition between central or effector memory subsets. Additionally, clonal interconversion was observed among central, effector memory and CD4 T cells re-expressing CD45RA cell subsets. Conversely, MUD/conventional HCT recipients demonstrated limited clonal plasticity, including clonal interconvention over time, consistent with findings in healthy adults. Moreover, the plasticity rate was independent of GVHD development, suggesting that early transplant decisions are the driving force for clonal behavior of reconstituting CD4 T cells over time. Conclusion: These data suggest that the clonal bottleneck observed after PTCy may be due entirely to the loss of naive T cells rather than a fundamental shift in the clonal diversity of effector and memory T cells in circulation. Our data further suggest that the phenotype of post-haplo/PTCy non-naive cells–although similar in clonality to MUD/MTX–is biased towards the effector memory state, with increased rates of clonal conversion between the dominant CD4 T cell memory phenotypes. These findings may underpin infectious risk after allo-HCT with PTCy and suggest that CD4 T cell reconstitution is substantially altered by early transplant decisions.

  PublisherDOI

• CXCR5⁺PD-1⁻ circulating T follicular helper cells identify vaccine readiness in pediatric allogeneic hematopoietic cell transplantation

  Blood · 2025-11-03

  articleOpen accessSenior author

  Abstract Background:&amp;#x2028;Children undergoing allogeneic hematopoietic cell transplantation (allo-HCT) are highly susceptible to vaccine-preventable infections due to prolonged delays in immune reconstitution. Current revaccination guidelines vary widely but typically rely on a combination of time from transplant and clinically available, broad measures of immune reconstitution. Unfortunately, many individuals continue to have poor vaccine response. Individualized measures of vaccine readiness are needed to optimize the timing of and response to vaccination. CD4+ circulating T follicular helper (cTfh) cells, defined by CXCR5 expression, are a promising candidate to predict vaccine readiness. Tfh are critical for germinal center function and long-lived antibody responses, and productive T:B cell interactions are required to generate normal frequency of cTfh. However, the dynamics of cTfh reconstitution after allo-HCT is not known, and the potential role of these cells in predicting vaccine readiness is not well established. Methods:&amp;#x2028;We conducted a prospective longitudinal study of pediatric patients at Children's Hospital of Philadelphia receiving SARS-CoV-2 mRNA vaccination following αβ T cell–depleted allo-HCT (n=11), alongside healthy controls (n=9) and solid organ transplant (SOT) recipients as immunosuppressed controls (n=22). Serial blood samples were collected pre- and post-vaccination. Vaccine responses were assessed by quantifying IgG against the receptor-binding domain (RBD) of the SARS-CoV-2 spike protein. Peripheral blood mononuclear cells (PBMCs) were analyzed by high-parameter spectral flow cytometry to characterize T and B cell reconstitution, including cTfh subsets (CXCR5⁺PD-1⁺ and CXCR5⁺PD-1⁻), functional Tfh1/Tfh17 polarization (CXCR3, CCR6), and memory B cells (CD27, IgD). Antigen-specific cellular responses were measured using flow cytometric activation-induced marker (AIM) assays and SARS-CoV-2 B cell probes. Results:&amp;#x2028;Serologic vaccine responses, measured by RBD-specific IgG, were impaired in allo-HCT recipients compared to healthy controls (p&amp;lt;0.01), while SOT recipients has variable non-responsiveness. Longitudinal sampling allowed for assessment of the recovery kinetics for CD4 T cell subpopulations. While CXCR5⁺PD-1⁺ cTfh cells recovered early in both groups, CXCR5⁺PD-1⁻ cTfh cells remained significantly reduced in allo-HCT recipients beyond 1.5 years post-transplant. Frequencies of CXCR5⁺PD-1⁻ cTfh cells were markedly lower in vaccine non-responders compared to responders in the HCT group (p&amp;lt;0.05), but not in SOT. In parallel, memory B cell recovery was also impaired in allo-HCT recipients who failed to respond to vaccination, with persistent reductions in both class-switched and unswitched CD27⁺ memory B cells. Interestingly, Tfh1-skewed cTfh polarization (CXCR3⁺) was associated with vaccine responsiveness in SOT recipients (p&amp;lt;0.05). CXCR5⁺PD-1⁻ cTfh showed strong correlation with serologic response (Spearman ρ = 0.72, p = 0.012) and whereas CXCR5⁺PD-1+ cTfh (ρ = 0.28, p = 0.41) did not. Moreover, CXCR5⁺PD-1⁻ cTfh also correlated significantly with the recovery of memory B cells (ρ = 0.79, p = 0.0092). These correlations were specific to the HCT group and not observed in the SOT. SARS-CoV-2-specific B cells were quantified using fluorescent spike and RBD probes. The frequency of the RBD+ memory B cells was reduced in HCT and was the lowest in the non respneders. Additionally, the presence of spike⁺ MBC cells positively correlated with CXCR5⁺PD-1⁻ cTfh frequencies (ρ = 0.78, p = 0.0068). Lastly, antigen-specific CD4⁺ T cell responses were assessed using activation-induced marker (AIM) assays (CD69⁺OX40⁺) following stimulation with SARS-CoV-2 peptide pools. Among allo-HCT recipients, 7/11 (64%) showed detectable CD4⁺ T cell responses. Conclusions:&amp;#x2028;Our findings suggest that CXCR5⁺PD-1⁻ cTfh cells are a key correlate of vaccine readiness in pediatric allo-HCT recipients. Our data suggest that reliance on fixed time intervals post allo-HCT may be insufficient to guide re-vaccination vaccination timing. Instead, individualized immune profiling using cTfh and B cell reconstitution could enable more effective vaccine timing. This approach has broad implications for clinical decision-making in transplant immunology, particularly as novel antigens and vaccines are introduced into post-transplant care. Larger prospective studies are needed to ensure generalizability across transplant protocols and across vaccine classes.

  PublisherOA PDFDOI

Recent grants

• Transcriptional and epigenetic regulation of Tfh dysfunction in HIV

  NIH · $778k · 2018–2023

Frequent coauthors

• E. John Wherry

  University of Pennsylvania

  205 shared

• Amy E. Baxter

  California University of Pennsylvania

  110 shared

• Josephine R. Giles

  University of Pennsylvania

  91 shared

• Sarah E. Henrickson

  University of Pennsylvania

  90 shared

• Cécile Alanio

  76 shared

• Allison R. Greenplate

  Translational Therapeutics (United States)

  71 shared

• Caroline Diorio

  Children's Hospital of Philadelphia

  69 shared

• Divij Mathew

  University of Pennsylvania

  69 shared

Labs

• Vella LabPI