Sarah Gaffen, PhD
- 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
Education & Training
- Postdoc, University of California San Francisco
- PhD, University of California Berkeley
- BS, Carnegie Mellon University
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 mucosal Candida albicans fungal infections, and (3) mechanisms by which dysregulated IL-17/Th17 cells drive pathogenesis of autoimmunity.
Gaffen SL, Moutsopoulos NM. 2020. Regulation of host-microbe interactions at oral mucosal barriers by type 17 immunity. Science Immunol. 5: eaau4594.
Li X, Bechara R, Zhao J, McGeachy M and Gaffen SL. 2019. IL-17 receptor based signaling and implications for diseases. Nature Immunol. 20: 1594-1602.
Amatya N, Childs EE, Cruz JA, Aggor FEY, Garg AV, Berman AJ, Gudjonsson JE, Atasoy U and Gaffen SL. 2018. IL-17 integrates multiple self-reinforcing, feed-forward mechanisms through the RNA-binding protein Arid5a. Science Signaling 11: eaat4617.
Verma AH, Richardson JP, Zhou C, Coleman BM, Moyes DL, Ho J, Huppler AR, Ramani K, McGeachy MJ, Mufazalov MA, Waisman A, Kane LP, Biswas PS, Hube B, Naglik JR and Gaffen SL. 2017. Oral epithelial cells orchestrate innate Type 17 responses to Candida albicans through the virulence factor Candidalysin. Science Immunol. 2: eaam8834.
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 and Gaffen SL. 2016. IL-17RA signaling in oral epithelium is critical for protection against oropharyngeal candidiasis. Cell Host & Microbe 20: 606-617.