Douglas McDonald, MD, PhD
Immunologist, Division of Immunology
Assistant Professor of Pediatrics, Harvard Medical School
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Douglas McDonald, MD, PhD
Immunologist, Division of Immunology
Assistant Professor of Pediatrics, Harvard Medical School
Medical Services
Languages
English
Education
Undergraduate School
Pennsylvania State University
State College
PA
Graduate School
Case Western Reserve University School of Medicine
Cleveland
OH
Medical School
Case Western Reserve University School of Medicine
Cleveland
OH
Internship
Cincinnati Children's Hospital
Cincinnati
OH
Residency
Cincinnati Children's Hospital
Cincinnati
OH
Fellowship
Allergy and Immunology
Boston Children's Hospital
Boston
MA
Certifications
American Board of Allergy & Immunology (General)
Publications
The role of dupilumab in the treatment of eosinophilic esophagitis. View Abstract
A Novel Combination of Compound Heterozygous Variants in IFNGR1 Causing Complete IFNGR1 Deficiency. View Abstract
Author Correction: DOCK8 functions as an adaptor that links TLR-MyD88 signaling to B cell activation. View Abstract
Inborn Errors of the Immune System Associated With Atopy. View Abstract
Immune dysregulation and multisystem inflammatory syndrome in children (MIS-C) in individuals with haploinsufficiency of SOCS1. View Abstract
Immunoglobulins in the treatment of COVID-19 infection: Proceed with caution! View Abstract
RIG-I and TLR4 responses and adverse outcomes in pediatric influenza-related critical illness. View Abstract
Impact of Gastroesophageal Reflux Disease on Mucosal Immunity and Atopic Disorders. View Abstract
Oral viscous mometasone is an effective treatment for eosinophilic esophagitis. View Abstract
Defective TLR9-driven STAT3 activation in B cells of patients with CVID. View Abstract
Hematopoietic stem cell transplantation outcomes for 11 patients with dedicator of cytokinesis 8 deficiency. View Abstract
Plasmacytoid dendritic cell depletion in DOCK8 deficiency: rescue of severe herpetic infections with IFN-a 2b therapy. View Abstract
Flow cytometry diagnosis of dedicator of cytokinesis 8 (DOCK8) deficiency. View Abstract
Intraoperative anaphylaxis to gelatin in topical hemostatic agents during anterior spinal fusion: a case report. View Abstract
DOCK8 functions as an adaptor that links TLR-MyD88 signaling to B cell activation. View Abstract
TH17 deficiency in human disease. View Abstract
Successful engraftment of donor marrow after allogeneic hematopoietic cell transplantation in autosomal-recessive hyper-IgE syndrome caused by dedicator of cytokinesis 8 deficiency. View Abstract
Clinical features and outcome of patients with IRAK-4 and MyD88 deficiency. View Abstract
Impaired T-cell receptor activation in IL-1 receptor-associated kinase-4-deficient patients. View Abstract
Immune deficiency caused by impaired expression of nuclear factor-kappaB essential modifier (NEMO) because of a mutation in the 5' untranslated region of the NEMO gene. View Abstract
Small-molecule screen identifies reactive oxygen species as key regulators of neutrophil chemotaxis. View Abstract
Heterozygous N-terminal deletion of IkappaBalpha results in functional nuclear factor kappaB haploinsufficiency, ectodermal dysplasia, and immune deficiency. View Abstract
Impaired immune response to vaccinia virus inoculated at the site of cutaneous allergic inflammation. View Abstract
Selective predisposition to bacterial infections in IRAK-4-deficient children: IRAK-4-dependent TLRs are otherwise redundant in protective immunity. View Abstract
Interleukin receptor-associated kinase-4 deficiency impairs Toll-like receptor-dependent innate antiviral immune responses. View Abstract
Lessons learned from molecular defects in nuclear factor kappaB dependent signaling. View Abstract
RIP links TLR4 to Akt and is essential for cell survival in response to LPS stimulation. View Abstract
A cell surface receptor complex for fibrillar beta-amyloid mediates microglial activation. View Abstract
beta-Amyloid fibrils activate parallel mitogen-activated protein kinase pathways in microglia and THP1 monocytes. View Abstract
Amyloid fibrils activate tyrosine kinase-dependent signaling and superoxide production in microglia. View Abstract
Locations