About

David Michael Allman, Ph.D., is a Professor of Pathology and Laboratory Medicine at the University of Pennsylvania. He serves as the Associate Director of the Abramson Cancer Center Flow Cytometry Core Facility and is the Vice Chair for Faculty Development in the Department of Pathology & Laboratory Medicine. His research focuses on studying various aspects of antibody-secreting plasma cells, which are the main source of antibodies throughout the body and play essential roles in host protection. His laboratory aims to define the biosynthetic pathways used by plasma cells to survive and maintain antibody titers, with the ultimate goal of eliminating pathogenic plasma cells involved in conditions such as chronic transplant rejection, autoimmunity, and multiple myeloma. Allman's work investigates how plasma cells activate, build up the endoplasmic reticulum to secrete large quantities of antibodies, and regulate ER function to sustain long-lived plasma cells. His research also explores how extrinsic factors in the bone marrow influence plasma cell survival, including mechanisms by which plasma cells perceive extracellular ATP via purinergic receptors. His contributions include advancing understanding of plasma cell biology, particularly in relation to their biosynthetic pathways, survival mechanisms, and implications for disease treatment.

Research topics

• Biology
• Virology
• Immunology
• Biochemistry
• Genetics

Selected publications

• Nanoparticle Immunoadjuvant Complexes Augment Germinal Center Responses to Vaccination

  Advanced Science · 2026-01-28

  articleOpen access

  Vaccine approaches capable of eliciting enhanced germinal center (GC) responses would result in improved protective humoral immunity against infectious diseases. Here, we investigate whether a cytokine can be scaffolded onto a self-assembling nanoparticle immunogen to enhance antigen-specific GC responses and B cell maturation. To test this approach, we design chimeric nanoparticles bearing eOD-GT8, a germline-targeting HIV immunogen, and IL-21, a canonical GC cytokine. DNA delivery of these nanoparticle immunoadjuvant complexes (GT8-IL-21-NICs) drives improved serum antibody titers and antigen-specific GC B cell responses in mice. Transcriptomic analysis of eOD-GT8-specific GC B cells demonstrates upregulation of selection-associated gene signatures with GT8-IL-21-NIC immunization. In mice harboring human bnAb precursor heavy and light chain genes, immunization with the GT8-IL-21-NIC leads to increased antibody diversity, clonal expansion, somatic hypermutation, and the acquisition of key antibody mutations. These results highlight IL-21 as a promising genetic adjuvant and demonstrate that NICs may be a valuable tool to improve antigen-specific GC responses and vaccine-induced immunity.

  PublisherOA PDFDOI

• The ancestral haplotype of P2RX5 yields a B-cell surface marker and a multi-lineage immunotherapy target

  bioRxiv (Cold Spring Harbor Laboratory) · 2026-01-14

  article

  SUMMARY While CD19- and BCMA-directed immunotherapies have improved outcomes for B-lymphoid and plasma cell malignancies, frequent relapses with antigen loss/downregulation highlight the need for new targets. Here, using transcriptomic datasets and newly-developed monoclonal antibodies, we show that P2RX5 , long considered a pseudogene in humans, encodes a stable protein in 80% of individuals of African descent carrying the ancestral haplotype. Like CD19, P2RX5 displays B-cell lineage-restricted expression in normal tissues. Unlike CD19, P2RX5 is expressed not only in B-cell neoplasms, but also in T-cell leukemia (T-ALL) and multiple myeloma (MM). We developed P2RX5-directed bispecific T-cell engagers and CAR T cells, which killed T-ALL cells with no evidence of T-cell fratricide. These agents were non-inferior to FDA-approved CD19- and BCMA-directed immunotherapeutics in cell culture and xenograft models of Burkitt lymphoma and MM, while maintaining potency against CD19- and BCMA-negative variants. Hence, P2RX5 is a unique multi-lineage target for frontline or salvage immunotherapy.

  PublisherDOI

• 63400 A randomized phase 2 proof-of-concept study to evaluate the efficacy and safety of topical bimiralisib application in patients suffering from actinic keratosis on the face and/or scalp and/or back of hands over a 2 and 4-week treatment period

  Journal of the American Academy of Dermatology · 2025-09-01

  article
  PublisherDOI

• Modulation of lipid nanoparticle-formulated plasmid DNA drives innate immune activation promoting adaptive immunity

  Cell Reports Medicine · 2025-03-22 · 19 citations

  articleOpen access

  T cell responses relative to mRNA-LNPs or adjuvanted protein, with memory responses persisting beyond one year. In rabbits immunized with HA DNA-LNP, we observed immune responses comparable or superior to mRNA-LNPs at the same dose. In an additional model, a SARS-CoV-2 spike-encoding DNA-LNP elicited protective efficacy comparable to spike mRNA-LNPs. Our study identifies a platform-specific priming mechanism for DNA-LNPs divergent from mRNA-LNPs or adjuvanted protein, suggesting avenues for this approach in prophylactic and therapeutic vaccine development.

  PublisherDOI

• Human Long-Lived Plasma Cells Acquire Resistance to Proteasome Inhibitor-Based Desensitization Treatment by Upregulating Autophagy

  American Journal of Transplantation · 2025-08-01

  article
  PublisherDOI

• Are human memory B cells ‘poised’ to become plasma cells? 4156

  The Journal of Immunology · 2025-11-01

  articleOpen accessSenior author

  Abstract Description During a recall immune response, memory B cells differentiate into plasma cells (PCs), which are indispensable for antibody production and humoral immunity. Furthermore, memory B cells proliferate sooner and require less stimulation to differentiate into PCs relative to naïve B cells and can thus be considered ‘poised’. The exact mechanisms explaining this discrepancy remain incompletely understood. Our lab has previously observed that mouse Marginal Zone (MZ) B cells are analogously ‘poised’ to become PCs relative to Follicular (FO) B cells. Transcriptomic analyses have shown that MZ B cells are enriched for hallmark mTORC1 signaling, unfolded protein response (UPR) pathway, and Myc target gene signatures compared to FO B cells, which are all required for PC differentiation. We hypothesized that these same gene signatures would be enriched in human memory B cells. From a cohort of healthy human donors, RNA-sequencing was performed on splenocytes. Indeed, we observe these same hallmark gene signatures enriched in memory B cells along with others involved in the synthesis of ribosomal proteins and translation. These results suggest that human memory B cells are better equipped to produce massive amounts of proteins that involve mTORC1 and Myc activity along with the UPR pathway, all of which are needed for antibody production by PCs. The better we understand PC differentiation mechanisms, the higher potential they can be manipulated for clinically relevant purposes. Funding Sources 5RO1AI175185-02 - Biochemical Mechanisms for Sustained Humoral Immunity Topic Categories Lymphocyte Differentiation and Peripheral Maintenance (LYM)

  PublisherOA PDFDOI

• Notch2 signaling instructs viral and bacterial TLR responsiveness in B cells

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-10-12

  preprintOpen accessSenior authorCorresponding

  Marginal zone (MZ) B cells are hyperresponsive to bacterial Toll-like Receptor (TLR) ligands. However, the full extent of TLR responsiveness for MZ B cells and the mechanisms regulating such responses are unclear. We report that Notch2 activation establishes MZ B cell responsiveness for the viral dsRNA receptor TLR3 and augments responses for the LPS receptor TLR4. Notch2 ligation accelerated Myc induction, mitosis, and plasma cell differentiation to LPS. Further, TLR3 expression in MZ B cells was Notch2 dependent, and ectopic Notch2 signaling was sufficient to promote robust TLR3 responsiveness dependent on the TIR-domain-containing adapter TRIF and the kinase BTK. TLR3 engagement in MZ B cells promoted proliferation, differentiation, and the secretion of IgG2b and IgG2c antibodies. Our results establish a novel role for Notch2 in establishing TLR3 and TLR4 responsiveness in B cells and suggest that MZ B cells play unappreciated roles in immunity against RNA viruses.

  PublisherOA PDFDOI

• Cell intrinsic versus cell extrinsic control of plasma cell longevity

  Trends in Immunology · 2025-11-24

  articleOpen access1st authorCorresponding
  PublisherOA PDFDOI

• Tailoring the adjuvanticity of lipid nanoparticles by PEG lipid ratio and phospholipid modifications

  Nature Nanotechnology · 2025-06-23 · 33 citations

  articleOpen access
  PublisherOA PDFDOI

• Notch2 signaling establishes a TLR response program in B cells 3708

  The Journal of Immunology · 2025-11-01

  articleOpen accessSenior author

  Abstract Description The efficiency with which B cells respond to activation signals varies by subset. Whereas marginal zone (MZ) B cells exhibit rapid activation following stimulation, follicular (FO) B cells adopt delayed effector programs. MZ B cells uniquely exhibit readiness for the plasma cell (PC) fate, differentiating in mere hours independent of mitosis or T cell help. These hallmarks are attributed to their TLR sensitivity; MZ B cells are hyperresponsive to bacterial signals and uniquely among B cells express TLR3, enabling a responsiveness to dsRNA. MZ B cells uniquely require constitutive signaling through the transmembrane receptor Notch2, but whether this signal underlies the functional poising of these cells is unclear. To examine the consequences of Notch2 on B cells with no Notch requirement, we co-cultured stimulated FO B cells on OP9 stromal cells expressing Notch2 ligand delta-like 1 (DL1). DL1 influenced TLR 3 and 4 responses in FO B cells by amplifying the time to first division and the propensity toward PC differentiation and class-switching altogether. Intriguingly, TLR3 responsiveness in B cells appeared to be entirely DL1-driven and dependent on Bruton’s Tyrosine Kinase. Employing a published mathematical model for dividing lymphocytes, we found Notch2 significantly augmented the division rate of activated B cells. Together, these observations demonstrate a novel role for Notch2 in instructing B cell response programs to TLR signals and their effector outcomes. Funding Sources Supported by NIH F31AI179166-01A1, R21AI174069-02, and T32-AI007632 Topic Categories Immune Response Regulation: Molecular Mechanisms (IRM)

  PublisherOA PDFDOI

Recent grants

• NIH Grant R21AI090700

  NIH · $422k · 2013

• NIH Grant R03AG020818

  NIH · $79k · 2003

• NIH Grant R01AI097590

  NIH · $1.9M · 2018

• NIH Grant R03AI053284

  NIH · $159k · 2004

• Origins of serum IgA antibodies

  NIH · $1.6M · 2014–2019

Frequent coauthors

• Warren S. Pear

  69 shared

• Susan Chan

  Inserm

  66 shared

• Philippe Kastner

  Institut de génétique et de biologie moléculaire et cellulaire

  66 shared

• Christine A. Biron

  64 shared

• S. H. Robbins

  Délégation Provence et Corse

  64 shared

• Marc Dalod

  Aix-Marseille Université

  64 shared

• Carine Asselin‐Paturel

  64 shared

• Thomas Delale

  64 shared

Labs

• Pathology and Laboratory MedicinePI

Education

• PhD, Immunology Graduate Group

  University of Pennsylvania

  1993