James Taylor | Howard Profiles

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Faculty

James G. Taylor, M.D.

Director

james.taylor2@Howard.edu

(202) 865-3118

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Department/Office

Center For Sickle Cell Disease

School/College

College of Medicine

Additional Positions

Professor

Internal Medicine
Professor

Microbiology

Biography

James G. Taylor VI, M.D., is a professor of microbiology who serves as Director of the Center for Sickle Cell Disease at Howard University. A board-certified pediatric hematologist/oncologist, Taylor earned his medical degree from the Medical College of Wisconsin, completed his residency in pediatrics at Washington University in St. Louis, and pursued advanced fellowships in pediatric hematology/oncology and genetics research at Johns Hopkins University and the National Institutes of Health (NIH). His academic training, including postdoctoral fellowships in vascular medicine and genomics at the NIH, positioned him to become a national leader in translational research on sickle cell disease.

Taylor’s clinical and research career has focused on the genetic and physiological underpinnings of pain in sickle cell anemia, particularly within African American populations. He has led groundbreaking studies on pain phenotyping, genetic admixture, and central sensitization in sickle cell disease, significantly advancing understanding of disease complications and informing more precise, personalized approaches to care. As director of a center that serves more than 350 adult sickle cell patients, Taylor oversees a multidisciplinary team of clinicians and scientists, helping bridge research and clinical care to reduce health disparities in hematologic disorders.

With prior roles at Johns Hopkins Hospital and the NIH, Dr. Taylor has received numerous honors, including the NIH Top Science Advance award and citations from the City of New York for his contributions to sickle cell advocacy. His scholarly output spans high-impact journals, and he has held influential roles on grant review panels, editorial boards, and advisory committees. Through his leadership at Howard University and as a co-investigator with the Center for Hemoglobin Research in Minorities (CHaRM), Taylor continues to champion equitable, research-driven solutions for patients historically underserved by the healthcare system.

Education

Post-doctoral Fellowship

Human Genetics Research
National Cancer Institute
2004

Fellowship

Pediatric Hematology/Oncology
Johns Hopkins University School of Medicine/NIH
2001

Residency

Pediatrics
Washington University, St. Louis
1998

Doctor of Medicine (M.D.)

Medicine
Medical College of Wisconsin
1995

Bachelor of Science (B.S.)

Biology
Creighton University
1991

Expertise

Hematology, sickle cell disease, genetics and genomics

Academics

Molecules and Cells course (M1)

Hematology/Medical Oncology Fellowship Program

Thalassemias; Hemoglobinopathies; Adult Acute Lymphoblastic Leukemia; Myelodysplastic Syndromes; Non-malignant Hematology Board Review

Research

Specialty

Disease specific research - sickle cell disease

Funding

P50 HL118006, NHLBI/NIH: Center for Hemoglobin Research in Minorities (CHarM)

Taylor, Robert E. (PI)

Role: Co-Investigator

10% effort (2017)

Faculty start-up Award (2017-2019): Howard University College of Medicine (Medicine) and Center for Sickle Cell Disease

Translational analysis of mechanisms of pain in sickle cell disease

Role: PI

Pfizer

RESET clinical trial

Role: PI

Accomplishments

2023 John Benjamin Nichols Award

Scientific Research and Service Award, Queens Sickle Cell Advocacy Network

Citation, Office of the President, Borough of Brooklyn, NY, 2014

Citation of Achievement, City Council, City of New York, 2014

Top Science Advance, NCI Center for Cancer Research, 2009

Featured News

Read: Diverse: Issues in Higher Education | Nobel Prize Spotlights Sickle Cell’s Disproportionate Impact on African Americans

Read: World Health Organization | Centre of excellence brings hope for sickle cell patients in Congo Republic

Publications and Presentations

Antiviral response and HIV-1 inhibition in sickle cell disease

Sickle cell disease (SCD) is characterized by hemolysis, vaso-occlusion, and ischemia. HIV-1 infection was previously shown to be suppressed in SCD PBMCs. Here, we report that HIV-1 suppression is attributed to the increased expression of iron, hypoxia, and interferon-induced innate antiviral factors.

Soluble urokinase-type plasminogen activator receptor

Soluble urokinase-type plasminogen activator receptor in sickle cell disease–associated chronic kidney disease

Renal manifestations are the most common complications of sickle cell disease (SCD). Renal disease starts during childhood and progresses further in adults.1 Approximately 30% of patients with SCD develop chronic kidney disease (CKD), and 14% to 18% of them progress to end-stage kidney disease. Thus, there is an urgent need to find specific biomarkers for the early detection of CKD in patients with SCD.

Routine Screening for Sickle Cell Disease during Pregnancy

Routine Screening for Sickle Cell Disease during Pregnancy: Epidemiological and Haemoglobin Profile in Congo

Sickle-cell disease, a genetic condition with a high prevalence in sub-Saharan Africa, is transmitted in an autosomal recessive mode. Its screening during pregnancy makes it possible to identify carriers of the S gene which constitute a risk for the unborn child. In order to promote the use of immuno-chromatographic tests, we have set ourselves the task of establishing the epidemiological profile and determining the Emmel test performance.

The gut microbiome in sickle cell disease

The gut microbiome in sickle cell disease: Characterization and potential implications

Sickle Cell Disease (SCD) is an inherited blood disorder that leads to hemolytic anemia, pain, organ damage and early mortality. It is characterized by polymerized deoxygenated hemoglobin, rigid sickle red blood cells and vaso-occlusive crises (VOC). Recurrent hypoxia-reperfusion injury in the gut of SCD patients could increase tissue injury, permeability, and bacterial translocation. In this context, the gut microbiome, a major player in health and disease, might have significant impact. This study sought to characterize the gut microbiome in SCD.

Association between plasma and urinary orosomucoid and chronic kidney disease

Association between plasma and urinary orosomucoid and chronic kidney disease in adults with sickle cell disease

Chronic kidney disease (CKD) strongly contributes to morbidity and mortality in ageing sickle cell disease (SCD) patients.1 Biomarkers for early stage CKD, such as proteinuria, microalbuminuria and reduced glomerular filtration rate (GFR), are difficult to detect in SCD patients because of a urine concentration defect. Thus, new biomarkers, which reflect the unique renal pathology of SCA-associated CKD, are needed for early detection and treatment.

Recent Articles

Multimedia

CGTN America | Dr. James Taylor discusses Howard University's fight against sickle cell disease

CGTN's Frances Kuo talks with Dr. James Taylor, director of the Center for Sickle Cell Disease at Howard University, about international collaboration in fighting the disease.