Physician

Allergy & Immunology

Joshua Milner works in the field of Allergy & Immunology. He graduated from Albert Einstein College of Medicine of Yeshiva University. Joshua Milner is also published. He has 38 publications published. The lastest publication: "Distinct Cutaneous Manifestations and Cold-Induced Leukocyte Activation Associated With PLCG2 Mutations.'

Publications

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• Distinct Cutaneous Manifestations and Cold-Induced Leukocyte Activation Associated With PLCG2 Mutations.
• Atopic Dermatitis in Children: Clinical Features, Pathophysiology, and Treatment.
• Early-onset lymphoproliferation and autoimmunity caused by germline STAT3 gain-of-function mutations.
• A mouse model of HIES reveals pro and anti-inflammatory functions of STAT3.
• Early-Onset Stroke and Vasculopathy Associated with Mutations in ADA2.
• Pathogen-Sensing, Regulatory T Cells, and Responsiveness-Tuning Collectively Regulate Foreign- and Self-Antigen Mediated T-Cell Responses.
• The cup runneth over: lessons from the ever-expanding pool of primary immunodeficiency diseases.
• Thymus transplantation restores the repertoires of forkhead box protein 3 (FoxP3)+ and FoxP3- T cells in complete DiGeorge anomaly.
• Dominant gain-of-function STAT1 mutations in FOXP3 wild-type immune dysregulation-polyendocrinopathy-enteropathy-X-linked-like syndrome.
• Mechanisms underlying helper T-cell plasticity: implications for immune-mediated disease.
• Peptide library-based evaluation of T-cell receptor breadth detects defects in global and regulatory activation in human immunologic diseases.
• Signal transducer and activator of transcription 1 (STAT1) gain-of-function mutations and disseminated coccidioidomycosis and histoplasmosis.
• HOIL and water: the two faces of HOIL-1 deficiency.
• Loss of mucosal CD103+ DCs and IL-17+ and IL-22+ lymphocytes is associated with mucosal damage in SIV infection.
• A Hypermorphic Missense Mutation in PLCG2, Encoding Phospholipase Cγ2, Causes a Dominantly Inherited Autoinflammatory Disease with Immunodeficiency.
• Cold Urticaria, Immunodeficiency, and Autoimmunity Related to PLCG2 Deletions.
• A critical role for STAT3 transcription factor signaling in the development and maintenance of human T cell memory.
• IL-17 producing cells in host defense and atopy.
• Altered T-cell receptor signaling in the pathogenesis of allergic disease.
• Highly variable clinical phenotypes of hypomorphic RAG1 mutations.
• Sustained IL-4 exposure leads to a novel pathway for hemophagocytosis, inflammation, and tissue macrophage accumulation.
• The characterization of twenty sequenced human genomes.
• Hypomorphic Rag mutations can cause destructive midline granulomatous disease.
• Cutting edge: lack of high affinity competition for peptide in polyclonal CD4+ responses unmasks IL-4 production.
• Th17 cells, Job's syndrome and HIV: opportunities for bacterial and fungal infections.
• Anaphylactic reaction to anakinra in a rheumatoid arthritis patient intolerant to multiple nonbiologic and biologic disease-modifying antirheumatic drugs.
• Autoimmunity in severe combined immunodeficiency (SCID): lessons from patients and experimental models.
• Exogenous vitamin D might contribute to geographic variations in epinephrine prescriptions.
• Lymphopenic mice reconstituted with limited repertoire T cells develop severe, multiorgan, Th2-associated inflammatory disease.
• Transient environmental exposures on the developing immune system: implications for allergy and asthma.
• Does the experience with the use of nasal continuous positive airway pressure improve over time in extremely low birth weight infants?
• Early infant multivitamin supplementation is associated with increased risk for food allergy and asthma.
• Does elevated peak bilirubin protect from retinopathy of prematurity in very low birthweight infants.
• The autoinhibitory C-terminal SH2 domain of phospholipase C-γ2 stabilizes B cell receptor signalosome assembly.
• Heterophile antibodies indicate progression of autoimmunity in human type 1 diabetes mellitus before clinical onset.
• Differential responses of invariant V alpha 24J alpha Q T cells and MHC class II-restricted CD4+ T cells to dexamethasone.
• Impaired T(H)17 cell differentiation in subjects with autosomal dominant hyper-IgE syndrome.

Schools

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• Albert Einstein College of Medicine of Yeshiva University

Doctors Specialties

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• Allergy
• Immunology

Accepted Insurances

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Education

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• National Institutes of Health Clinical Center
• Children's National Medical Center - George Washington University
• Albert Einstein College of Medicine of Yeshiva University

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