Faculty

Jonathan J Miner, M.D., Ph.D.

faculty photo
Associate Professor of Medicine (Rheumatology)
Department: Medicine
Graduate Group Affiliations

Contact information
522B Johnson Pavilion
3610 Hamilton Walk
Philadelphia, PA 19104
Office: 215-573-4109
Education:
B.A. (Russian)
BYU, 2002.
B.S. (Zoology)
BYU, 2002.
Ph.D. (Biochemistry and Molecular Biology)
University of Oklahoma, 2008.
M.D. (Medicine)
University of Oklahoma, 2010.
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Description of Clinical Expertise

Dr. Miner sees patients with rare autoinflammatory diseases and vasculopathies caused by single gene mutations. This includes RVCL (also known as RVCL-S), AGS, SAVI, COPA syndrome, and others.

Description of Research Expertise

The Miner laboratory studies the intersection of autoimmunity and antiviral immunity. This includes studies of rare rheumatic diseases caused by mutations in genes that regulate immune responses to viruses, such as the TREX1, cGAS, STING, RIG-I, and STAT1 genes.

The Miner laboratory is also developing novel therapeutics for rare diseases, including gene therapies and small molecular inhibitors, as well as whole-genome CRISPR/Cas9 screens to identify novel regulators of these pathways.

Examples of diseases studied in the Miner laboratory include:
* Retinal vasculopathy with cerebral leukoencephalopathy (RVCL), caused by mutations in TREX1.
* STING-associated vasculopathy with onset in infancy (SAVI), caused by mutations in STING.
* Chronic mucocutaneous candidiasis (CMC), caused by mutations in STAT1
* Monogenic systemic lupus erythematosus (SLE), caused by mutations in NF-kB signaling pathways
* Hemophagocytic lymphohistiocytosis (HLH), caused by mutations in viral RNA-sensing pathways
* Viral infections (e.g., models of chikungunya viral arthritis, and models of Zika virus, West Nile virus, bunyavirus, coronavirus, and herpesvirus pathogenesis).

Selected Publications

Platt DJ, Lawrence D, Qian W, Rodger R, Schriefer L, Miner CA, Menos AM, Kennedy EA, Peterson ST, Stinson WA, Baldridge MT, Miner, JJ: Transferrable protection by gut microbes against STING-associated lung disease. Cell Rep 35(6): 109133, May 2021.

Bennion BG, Croft CA, Ai TL, Qian W, Menos AM, Miner CA, Fremond ML, Doisne JM, Andhey PS, Platt DJ, Bando JK, Wang ER, Luksch H, Molina TJ, Robison EDO, Artyomov MN, Rosen-Wolff A, Colonna M, Rieux-Laucat F, Di Santo JP, Neven B, Miner JJ. : STING gain-of-function disrupts lymph node organogenesis and innate lymphoid cell development in mice. Cell Rep. 31(11): 107771, Jun 2020.

Luksch H, Stinson WA, Platt DJ, Qian W, Kalugotla G, Miner CA, Bennion BG, Gerbaulet A, Rösen-Wolff A, Miner JJ.: STING-associated lung disease in mice relies on T cells but not type I interferon. J Allergy Clin Immunol. 144(1): 154-266, July 2019.

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Last updated: 07/10/2024
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