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_IMG_4948.JPG Sarah Gaffen , Ph.D.
Professor of Medicine
S702 BST South
Pittsburgh, PA 15261
Phone: 412-383-8903
Email: sig65@pitt.edu
Fax: 412-383-8864
Faculty Research Interests
Personal Web Page
 
Research Interests
T cell derived cytokines are critical for mediating host defense against infectious disease, but they also mediate disease pathology in autoimmunity. In the last few years a new type of CD4+ T cells has been discovered that plays a key role in autoimmunity. Distinct from the classic Th1 and Th2 populations, these cells are termed "Th17" based on production of the signature effector cytokine IL-17. IL-17 and its receptor are unique in structure and sequence from other known cytokines, and the Gaffen lab was among the first to study signaling mechanisms mediated by this this novel family of cytokines. Our group takes a variety of biochemical, molecular and in vivo approaches to defining IL-17-mediated signaling, with an emphasis on defining its biological function in the oral mucosa and in autoimmune disease.
 
Academic Affiliation
Division of Rheumatology & Clinical Immunology
University of Pittsburgh School of Medicine
 
Selected Publications
Gaffen SL. Structure and signalling in the IL-17 receptor family. Nature Reviews Immunology, 2009; 9:556-67.

Conti HR, Shen F, Nayyar N, Stocum E, Sun JN, Lindemann MJ, Ho AW, Hai JH, Yu JJ, Jung JW, Filler SG, Masso-Welch P, Edgerton M, Gaffen SL. Th17 cells and IL-17 receptor signaling are essential for mucosal host defense against oral candidiasis. J Exp Med, 2009; 206:299-311

Shen F, Li N, Gade P, Kalvakolanu D, Weibley T, Doble B, Woodgett JR, Wood TD, Gaffen SL. IL-17 receptor signaling inhibits C/EBP by sequential phosphorylation of the regulatory 2 domain. Science Signaling, 2009; 2:ra8.

Ho AW, Shen F, Conti HR, Patel N, Childs EE, Peterson AC, Hernández-Santos N, Kolls JK, Kane LP, Ouyang W, Gaffen SL. IL-17RC is required for immune signaling via an extended SEFIR domain in the cytoplasmic tail. J. Immunol, 2010; 185:1063-70.

Conti HR, Baker O, Freeman AF, Holland SM, Jang WS, Li RA, Edgerton M, Gaffen SL. New mechanism of oral immunity to mucosal candidiasis in Hyper-IgE syndrome. Mucosal Immunol, 2011; 4:448-455.

Pandiyan P, Conti HR, Zheng L, Peterson AC, Mathern D, Hernández-Santos N, Edgerton M, Gaffen SL, Lenardo MJ. CD4+CD25+Foxp3+ regulatory T cells promote Th17 cells in vitro and enhance host resistance in mouse Candida albicans Th17 infection model. Immunity, 2011; 34:422-34.

Hernández-Santos N, Gaffen SL. Th17 immunity to Candida albicans. Cell Host Microb, 2012; 11:425-435.

Hernández-Santos N, Huppler AR, Peterson AC, Khader S, McKenna K, Gaffen SL. IL-17-producing T cells confer long term adaptive immunity to Candida albicans. Mucosal Immunol, 2013; 6:900-910.

Garg A, Ahmed M, Vallejo A, Ma A, Gaffen SL. The deubiquitinase A20 mediates feedback inhibition of Interleukin-17 receptor signaling. Science Signaling, 2013; 6:ra44.

Ho A, Garg AV, Monin L, Simpson-Abelson MR, Kinner L, Gaffen SL. The anaphase promoting complex 5 (AnapC5) associates with A20 and inhibits IL-17-mediated signal transduction. PLoS One, 2013; 8:e70168.
 
Grants
R01-AR054389 “Structure Function Relationships in the IL-17 Receptor” 2008-13 (NCE 2013-14)

R01-DE022550 “IL-17R signaling in the Oral Mucosa” 2012-17

Novartis “IL-17 Blockade and Opportunistic Candida infections” 2012-14
 
 


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