Nathan Archer, Ph.D.
Ph.D. – University of Maryland at Baltimore
Assistant Professor
Department of Dermatology
Johns Hopkins University School of Medicine
Cancer Research Building II – 2M04
Baltimore, MD. 21231
Phone: (410) 614-3490
E-mail: [email protected]
Research:
Keywords: bacteria, dermatology, innate/adaptive responses, inflammation, allergic disease, immunotherapy, Staphylococcus aureus
Research Activities
Our lab seeks to understand the immune mechanisms that protect against skin pathogens and promote inflammatory skin diseases, which can serve as targets for the development of novel immune-based therapeutics.
Summary of Research Program
Our goal is to understand mechanisms of protective innate and adaptive immune responses to skin pathogens and the role of aberrant immune responses and the skin microbiome in the pathogenesis of inflammatory skin diseases, including atopic dermatitis and psoriasis. We have made discoveries involving Toll-like receptors (TLRs), IL-1 family cytokines, inflammasome responses, and the role of different T cell subsets (especially IL-17-producing T cells). We are currently investigating the protective immunity to Staphylococcus aureus, which is the most common human bacterial skin pathogen. This area of research is highly significant since S. aureus infections represent a major public health threat due to the widespread emergence of virulent community-acquired methicillin-resistant S. aureus (MRSA) strains. In our work involving pathogenic immune mechanisms and dysbiosis of the skin microbiome in contributing to skin inflammation and allergic disease, we have made key discoveries involving the role of IL-36, MyD88-signaling, and STAT3-signaling. Our long-term goal is to discover mechanisms that can serve as targets for future immune-based therapies and vaccination strategies.
Publications and Interests: https://jhu.pure.elsevier.com/en/persons/nathan-archer
Learn More
Contact Us
Miller Research Building
Suite 631
733 North Broadway
Baltimore, Maryland 21205
Office: (410) 955-2709
Email: [email protected]
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