Betsy J. Barnes, PhD
Barnes LabLaboratory of Autoimmune and Cancer Research
Phone(516) 562-0434
Research & opportunities
The Pediatric Hematology and Oncology Labs investigate red-cell development, immune regulation, and cancer.
Research area
Developmental erythropoiesis
How red blood cells develop—from early progenitors to mature cells—and how ribosomal defects disrupt this process in inherited anemia.
The Blanc lab combines studies of human erythroid cells with experimental models of blood disorders. Recent work maps protein and cell-cycle changes across red-cell development and shows how deficiencies in the ribosomal proteins RPS19 and RPL5 affect fetal blood formation through distinct mechanisms in mouse models of Diamond-Blackfan anemia syndrome.
- Erythroid progenitors
- Reticulocyte maturation
- Ribosome biology
- Diamond-Blackfan anemia syndrome
Selected research
Ribosomes and the origins of blood
Mouse models of RPS19 and RPL5 deficiency reveal distinct disruptions to fetal blood formation, informing research into Diamond-Blackfan anemia syndrome.
Read the paperThe final steps of red-cell maturation
Analyses of human bone-marrow reticulocytes map changes in proteins, organelles, and membrane properties as these cells mature into red blood cells.
Read the paperResearch area
Autoimmunity & inflammation
How IRF5 and its signaling partners regulate inflammation, and how immune responses affect tissues and blood formation in autoimmune disease.
The Barnes lab studies the molecular control of immune-cell activity, including the STK25–IRF5 pathway. Collaborative work examines inflammatory marrow niches in lupus-prone mice and links a gut bacterial lipoglycan to thromboinflammation in lupus nephritis through patient observations and mouse experiments. These studies connect immune regulation with the tissue environments in which disease develops.
- IRF5 signaling
- Systemic lupus erythematosus
- Inflammatory marrow niches
Selected research
A molecular switch in inflammatory signaling
The study identifies STK25 as a regulator of IRF5 activation and inflammatory signaling, using biochemical assays, human immune cells and mouse immune-cell models.
Read the paperInflammation in the blood-forming niche
In lupus-prone mice, human TLR8 expression alters the marrow environment that supports red-cell production and is associated with severe anemia.
Read the paperGut microbes and lupus inflammation
A collaborative study links a gut bacterial lipoglycan to platelet and neutrophil activation in lupus nephritis, combining patient observations with mechanistic experiments in mice.
Read the paperResearch area
Cancer & immune biology
How tumor signaling and extracellular vesicles influence metastatic environments, and how tumor antigens can be explored as targets for immunity.
Work coauthored by Betsy J. Barnes and Lionel Blanc examines IRF5, tumor-derived extracellular vesicles, and pre-metastatic niche formation in breast-cancer and osteosarcoma models. Complementary research led by Betsy J. Barnes uses human expression datasets to identify cancer-testis antigens, then tests peptide vaccines in a mouse model of triple-negative breast cancer. These are mechanistic and preclinical studies.
- Tumor-derived extracellular vesicles
- Metastatic niches
- Cancer-testis antigens
Selected research
How tumors shape sites of metastatic spread
In breast-cancer and osteosarcoma models, the study examines how IRF5 shapes tumor-derived extracellular vesicles and the environments that support metastatic spread.
Read the paperTesting targets for antitumor immunity
Public human expression datasets guide the selection of cancer-testis antigens, followed by peptide-vaccine experiments in a mouse model of triple-negative breast cancer.
Read the paperContact
For scientific conversations, collaborations, and future opportunities with either lab.
Feinstein Institutes for Medical Research
Lionel Blanc, PhD
Blanc LabLaboratory of Developmental Erythropoiesis
Emaillblanc@northwell.edu
Phone(516) 562-1507
Opportunities
Confirmed openings and application instructions will appear here when available.