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The Nathan K. Archer Laboratory

Welcome to the Nathan K. Archer Laboratory at the Johns Hopkins Department of Dermatology.

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.

Our research has used innovative in vivo preclinical models, including pioneering advanced techniques of in vivo whole animal optical (bioluminescence and fluorescence) imaging to track bacterial clearance and host immune responses noninvasively and longitudinally over time, human skin organotypic culture models and novel humanized mouse models possessing both human skin and immune cells. Our laboratory has been funded with NIH grant support (R01 and K01 grants) and extensive industry and foundation support.

In addition to our work in the skin, we are investigating protective immune responses and novel antibacterial coatings to help treat or prevent bacterial biofilm-related infections of medical devices, prostheses, and implants. These infections are a devastating complication as bacterial biofilms form on the foreign implanted materials, which inhibit the efficacy of antibiotics and blocks penetration of immune cells. We have multiple preclinical animal models of these post-surgical infections using the latest technology in multimodality imaging, including optical, PET, CT, and photoacoustic imaging. The goal is to provide new insights into protective immune responses and novel treatments against these biofilm-related implant infections.

Please contact us if you would like to learn more about our work.

A graphical abstract representing Staphylococcus aureus colonization during atopic dermatitis contributing to skin inflammation.Staphylococcus aureus colonization during atopic dermatitis contributes to skin inflammation, but the underlying mechanisms are unclear. Our research demonstrates that epicutaneous S. aureus exposure drives skin inflammation, which is mediated by the bacterial PSMα and host IL-36R/MyD88-induced production of IL-17 by T cells.
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