- ASSISTANT PROFESSOR Medicine, Clinical Immunology
Specific Clinical/Research Interest:
Inflammation is a very important component of the host response to infections and tumors. However, excessive inflammation may lead to a variety of pathological states, including different autoimmune disorders.
The main interest of our lab is focused on understanding the cellular and molecular basis that lead to the induction, development and resolution of inflammatory disorders that are caused by the dysfunctions of the innate and/or the adaptive immune system.
In particular, we are interested in the study of the TH17 cells, a recently identified CD4+ T cell subset distinct from T helper type 1 (TH1) and T helper type 2 (TH2) cells. TH17 cells can drive antigen specific autoimmune diseases and are considered the main population of pathogenic T cells driving experimental autoimmune encephalomyelitis (EAE), the mouse model for multiple sclerosis. The factors that are needed for the generation of TH17 cells have been well characterized. However, where and how the immune system controls TH17 cells in vivo is one of our major interests.
To address these questions, our laboratory employs a wide range of experimental techniques to get insight from epigenetics (FISH, 3C, ChIP, EMSA, DHA, genome wide gene expression analyses…) to the whole animal level (genetic approaches including conditional targeting and generation of different reporter mice).
Development of autoimmune diabetes in the absence of detectable IL-17A in a CD8-driven virally induced model.
Van Belle TL*, Esplugues E*, Liao J, Juntti T, Flavell RA, von Herrath MG.
J Immunol. 2011 Sep 15;187(6):2915-22 (*co-first authors)
Control of TH17 cells occurs in the Small Intestine.
Esplugues E*#, Huber S*, Gagliani N, Hauser AE, Town T, Wan YY, O’Connor Jr. W, Rongvaux A, Van Rooijen N, Haberman AM, Iwakura Y, Kuchroo VK, Kolls JK, Bluestone JA, Herold KC, Flavell RA#.
Nature. 2011 Jul 17; 475(7357):514-8. (*co-first authors, #co-directed the project)
F1000 Article Factor: 16
miR-33a/b contribute to the regulation of fatty acid metabolism and insulin signaling.
Dávalos A, Goedeke L, Smibert P, Ramírez CM, Warrier NP, Andreo U, Cirera-Salinas D, Rayner K, Suresh U, Pastor-Pareja JC, Esplugues E, Fisher EA, Penalva LO, Moore KJ, Suárez Y, Lai EC, Fernández-Hernando C.
Proc Natl Acad Sci U S A. 2011 May 31;108(22):9232-7
TH17 Cells Express Interleukin-10 Receptor and Are Controlled by Foxp3(-) and Foxp3(+) Regulatory CD4(+) T Cells in an Interleukin-10-Dependent Manner.
Huber S*, Gagliani N*, Esplugues E*,O'Connor W Jr, Huber FJ, Chaudhry A, Kamanaka M, Kobayashi Y, Booth CJ, Rudensky AY, Roncarolo MG, Battaglia M, Flavell RA.
Immunity. 2011 Apr 22;34(4):554-65. (*co-first authors)
F1000 Article Factor: 8
CD69 limits early inflammatory diseases associated with immune response to Listeria monocytogenes infection.
Vega-Ramos J, Alari-Pahissa E, Valle JD, Carrasco-Marín E, Esplugues E, Borràs M, Martínez-A C, Lauzurica P.
Immunol Cell Biol. 2010 Oct;88(7):707-15.
CD69 targeting differentially affects the course of collagen-induced arthritis.
Sancho D, Gómez M, Martinez Del Hoyo G, Lamana A, Esplugues E, Lauzurica P, Martinez-A C, Sánchez-Madrid F.
J Leukoc Biol. 2006 Dec;80(6):1233-41.
The adaptor protein 3BP2 binds human CD244 and links this receptor to Vav signaling, ERK activation, and NK cell killing.
Saborit-Villarroya I, Del Valle JM, Romero X, Esplugues E, Lauzurica P, Engel P, Martín M.
J Immunol. 2005 Oct 1;175(7):4226-35.
Induction of tumor NK-cell immunity by anti-CD69 antibody therapy.
Esplugues E, Vega-Ramos J, Cartoixà D, Vazquez BN, Salaet I, Engel P, Lauzurica P.
Blood. 2005 Jun 1;105(11):4399-406.
Identification and characterization of a novel spliced variant that encodes human soluble tumor necrosis factor receptor 2.
Lainez B, Fernandez-Real JM, Romero X, Esplugues E, Cañete JD, Ricart W, Engel P.
Int Immunol. 2004 Jan;16(1):169-77.
CD69 downregulates autoimmune reactivity through active transforming growth factor-beta production in collagen-induced arthritis.
Sancho D, Gómez M, Viedma F, Esplugues E, Gordón-Alonso M, García-López MA, de la Fuente H, Martínez-A C, Lauzurica P, Sánchez-Madrid F.
J Clin Invest. 2003 Sep;112(6):872-82.
F1000 Article Factor: 8
Enhanced antitumor immunity in mice deficient in CD69.
Esplugues E, Sancho D, Vega-Ramos J, Martínez C, Syrbe U, Hamann A, Engel P, Sánchez-Madrid F, Lauzurica P.
J Exp Med. 2003 May 5;197(9):1093-106.
F1000 Article Factor: 9
CD84 functions as a homophilic adhesion molecule and enhances IFN-gamma secretion: adhesion is mediated by Ig-like domain 1.
Martin M, Romero X, de la Fuente MA, Tovar V, Zapater N, Esplugues E, Pizcueta P, Bosch J, Engel P.
J Immunol. 2001 Oct 1;167(7):3668-76.
Physicians and scientists on the faculty of the Icahn School of Medicine at Mount Sinai often interact with pharmaceutical, device and biotechnology companies to improve patient care, develop new therapies and achieve scientific breakthroughs. In order to promote an ethical and transparent environment for conducting research, providing clinical care and teaching, Mount Sinai requires that salaried faculty inform the School of their relationships with such companies.
Dr. Esplugues did not report having any of the following types of financial relationships with industry during 2014 and/or 2015: consulting, scientific advisory board, industry-sponsored lectures, service on Board of Directors, participation on industry-sponsored committees, equity ownership valued at greater than 5% of a publicly traded company or any value in a privately held company. Please note that this information may differ from information posted on corporate sites due to timing or classification differences.
Mount Sinai's faculty policies relating to faculty collaboration with industry are posted on our website at http://icahn.mssm.edu/about-us/services-and-resources/faculty-resources/handbooks-and-policies/faculty-handbook. Patients may wish to ask their physician about the activities they perform for companies.
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Icahn Medical Institute Floor 11 Room 20D
1425 Madison Avenue
New York, NY 10029