Alicia R. Mathers, PhD
Campus: 200 Lothrop St
Office: W1156 BSTWR
Lab: W1104 BSTWR
Pittsburgh, PA 1561
- PhD, West Virginia University
- Assistant Professor, Department of Dermatology
- Assistant Professor, Department of Immunology
The focus of our laboratory is to understand how cutaneous inflammation is induced and to exploit that knowledge to develop novel therapeutics utilizing both murine and human models.
In our first project we are examining the role of danger signals, specifically ATP/P2X7R, in the development and maintenance of psoriatic lesions. We have determined that signaling through the P2X7R in vitro leads to the differentiation of Th17 cells, utilizing both human and murine cells. Moreover, if P2X7R agonists are injected into the skin we can induce an acute psoriasis-like response in mice, indicating that ATP/P2X7R likely has a role in initiating the development of psoriasis lesions.
In our second project, we have determined that an exemplary electrophilic nitro fatty acid, nitro oleic acid (OA-NO2), has the capacity to suppress contact hypersensitivity responses, we hope to eventually translate this finding into psoriasis models. Furthermore, we are focused on understanding the mechanisms by which OA-NO2 suppresses cutaneous inflammation in order to better understand these inflammatory processes.
To explore pertinent questions of cutaneous biology, our laboratory has utilized human skin explants and murine models of disease. We also perform human to mouse skin xenotransplants with biopsies that we have collected from healthy human skin and (non)psoriatic lesional skin.
The Mathers lab has two R01 funded projects (2016-2020) to study cutaneous inflammation and psoriasis. Graduate students interested in rotation opportunities should contact Dr. Mathers.
Monin L, Gudjonsson JE, Childs EE, Amatya N, Xing X, Verma AH, Coleman BM, Killeen M, Mathers A, Ward NL, and SL Gaffen. (2017) MCPIP1/Regnase-1 restricts IL-17A- and IL-17C-dependent skin inflammation. J Immunol. 198(2):767-775. PMID: 27920272
Mathers AR. (2016) Commentary: TREX through cutaneous health and disease. J Invest Dermatol. 136(12):2337-2339. PMID:27884288
Mathers AR*, Carey CD, Killeen ME, Diaz-Perez J., Salvatore SR, Schopfer FJ, Freeman BA, and LD Falo Jr. Electrophilic nitro-fatty acids suppress allergic contact dermatitis. Allergy. Accepted doi:10.1111/all.13067 (Epub ahead of print). PMID: 27718238
Korkmaz E, Friedrich EE, Ramadan MH, Erdos G, Mathers AR, Ozdoganlar OB, Washburn NR, and LD Falo Jr. (2015) Therapeutic intradermal delivery of tumor necrosis factor-alpha antibodies using tip-loaded dissolvable microneedle arrays. Acta Biomater. 24: 96-105. PMID: 26093066
*†Killeen M, Ferris LK, Kupetsky EA, Falo LD Jr, and AR Mathers (2013) Signaling through Purinergic Receptors for ATP Induces Human Cutaneous Innate and Adaptive Th17 Responses: Implications in the Pathogenesis of Psoriasis. J. Immunol. 190:4324-36. PMID: 23479230
* featured in the “In This Issue” section of The Journal of Immunology. “In This Issue” highlights articles that are among the top 10% of articles published in the journal.
†selected as an ‘Editors Pick’ in the Journal of Investigative Dermatology (2013) 133: 1917.
Kupetsky EA, Mathers AR and LK Ferris. (2013) Cytokine-Targeted Therapy in the Treatment of Psoriasis. Cytokine 61:704-12. PMID: 23410503
Mathers AR, Janelsins BM, Rubin JP, Tkacheva OA, Morelli AE, and AT Larregina. (2009) Differential capability of human cutaneous dendritic cell subsets to initiate Th17 responses. J. Immunol. 182:921-33. PMID: 19124735
Mathers AR, Tkacheva OA, Janelsins BM, Shufesky WJ, Morelli AE, and AT Larregina. (2007) In vivo signaling through the neurokinin 1 receptor favors transgene expression by Langerhans cells and promotes the generation of Th1- and Tc1-biased immune responses. J. Immunol. 178: 7006-7017. PMID: 17513750
Click here for a complete list of publications.
- Understanding induction of cutaneous inflammation, in particular psoriasis
- Develop novel therapeutics utilizing both murine and human models