Sarah Gaffen, PhD

Sarah Gaffen, PhD

Contact

S702 Biomedical Science Tower South
200 Lothrop Street
Pittsburgh, PA 15213

Ph: 412-383-8903

Fax: 412-383-8864

sarah.gaffen@pitt.edu

My Website »

Education

  • Postdoc, University of California at San Francisco
  • PhD, University of California at Berkeley
  • BS, Carnegie Mellon University

Academic Affiliation

Gerald P. Rodnan Professor, Department of Medicine, Division of Rheumatology & Clinical Immunology

Professor, Department of Immunology

Director, Basic Rheumatology Research

Member, Graduate Program in Microbiology and Immunology (PMI)

Member, Molecular Genetics and Developmental Biology Graduate Program

About Research

T cell derived cytokines are critical for mediating host defense against infectious disease, but they also mediate disease pathology in autoimmunity. A subset of CD4+ T cells, known as "Th17 cells" based on production of the cytokine IL-17, plays a key role in driving autoimmunity. Conversely, IL-17 and Th17 cells play important roles in fungal immunity, particularly in protection against opportunistic mucosal infections caused by the commensal yeast Candida albicans,first shown by Dr. Gaffen's group. IL-17 and its receptor are unique in structure and sequence from other known cytokines, and the Gaffen lab has been a leader in studying signaling pathways mediated by this this novel family of cytokines. In addition, antibodies against IL-17 and its receptor were recently approved by the FDA to treat autoimmune conditions, particularly psoriasis.

The Gaffen lab studies three aspects of IL-17/Th17 cell biology: (1) mechanisms of molecular signal transduction mediated by IL-17 and its receptor (2) means by which IL-17 mediates host defense against mucosalCandida albicans fungal infections, and (3) mechanisms by which dysregulated IL-17/Th17 cells drive pathogenesis of autoimmunity. 

Selected Publications

Amatya N, Cruz JA, Aggor FEY, Garg AV, Berman AJ, Atasoy U and Gaffen SL. 2018. IL-17 integrates multiple self-reinforcing, feed-forward signaling cascases through the RNA-binding protein Arid5a. Science Signaling in press.

Verma AH, Richardson JP, Moyes DL, Ho J, Huppler AR, Ramani K, Coleman BM, Kane LP, Biswas PS, Hube B, Naglik JR, Gaffen SL. 2017. Oral epithelial cells orchestrate innate Type 17 responses to Candida albicans through the virulence factor Candidalysin. Science Immunology. 2: eaam8834 (Featured Cover Art)

Amatya N, Garg AV, Gaffen SL. 2017. The Yin and the Yang of IL-17 signaling. Trends Immunol. 38: 310-322. (Fectured Cover Art)

Conti HR, Bruno VM, Childs EC, Daugherty S, Hunter JP, Mengesha BG, Saevig DL, Hendricks MR, Coleman BM, Brane L, Solis N, Cruz JA, Verma AH, Garg AV, Hise AG, Richardson JP, Naglik JR, Filler SG, Kolls JK, Sinha S, Gaffen SL. 2016. IL-17RA signaling in oral epithelium is critical for protection against oropharyngeal candidiasis. Cell Host & Microbe. 20: 606-617.

Garg AV, Amatya N, Chen K, Cruz JA, Grover P, Whibley N, Conti HR, Mir GH, Sirakova T, Childs EC, Smithgall TE, Biswas PS, Kolls JK, McGeachy MJ, Kollatukudy PE, Gaffen SL. 2015. MCPIP1 endoribonuclease activity negatively regulates interleukin-17-mediated signaling and inflammation. Immunity. 43: 475-487.

Click here for a full list of publications>