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Enric Esplugues, PhD

Associate Research Scientist

Contact Information

Enric Esplugues, PhD

Lab Location

Mailing Address

  • The Anlyan Center

    300 Cedar Street

    New Haven, CT 06519

    United States

Research Summary

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).

Coauthors

Research Interests

Autoimmune Diseases; Immune System Diseases; Autoimmunity

Public Health Interests

Cancer; Nutrition

Selected Publications

  • Intestinal Tr1 cells migrate to periphery to suppress diabetogenic T cells and prevent diabetes development.Yu H , Gagliani N , Ishigame H , Huber S, Zhu S , Esplugues E , Herold KC , Wen L , Flavell RA. PNAS. 2017
  • TH17 cells express ST2 and are controlled by the alarmin IL-33 in the small intestine.Pascual-Reguant A, Bayat Sarmadi J, Baumann C, Noster R, Cirera-Salinas D, Curato C, Pelczar P, Huber S, Zielinski CE, Löhning M, Hauser AE, Esplugues E. TH17 cells express ST2 and are controlled by the alarmin IL-33 in the small intestine. Mucosal Immunology 2017, 10: 1431-1442. PMID: 28198366, DOI: 10.1038/mi.2017.5.
  • TFH cells progressively differentiate to regulate the germinal center response.Weinstein JS, Herman EI, Lainez B, Licona-Limón P, Esplugues E, Flavell R, Craft J. TFH cells progressively differentiate to regulate the germinal center response. Nature Immunology 2016, 17: 1197-1205. PMID: 27573866, PMCID: PMC5030190, DOI: 10.1038/ni.3554.
  • Apoptosis in response to microbial infection induces autoreactive TH17 cells.Campisi L, Barbet G, Ding Y, Esplugues E, Flavell RA, Blander JM. Apoptosis in response to microbial infection induces autoreactive TH17 cells. Nature Immunology 2016, 17: 1084-92. PMID: 27455420, PMCID: PMC5079524, DOI: 10.1038/ni.3512.
  • Th17 cells transdifferentiate into regulatory T cells during resolution of inflammation.Gagliani N, Amezcua Vesely MC, Iseppon A, Brockmann L, Xu H, Palm NW, de Zoete MR, Licona-Limón P, Paiva RS, Ching T, Weaver C, Zi X, Pan X, Fan R, Garmire LX, Cotton MJ, Drier Y, Bernstein B, Geginat J, Stockinger B, Esplugues E, Huber S, Flavell RA. Th17 cells transdifferentiate into regulatory T cells during resolution of inflammation. Nature 2015, 523: 221-5. PMID: 25924064, PMCID: PMC4498984, DOI: 10.1038/nature14452.
  • Dynamic signaling by T follicular helper cells during germinal center B cell selection.Shulman Z, Gitlin AD, Weinstein JS, Lainez B, Esplugues E, Flavell RA, Craft JE, Nussenzweig MC. Dynamic signaling by T follicular helper cells during germinal center B cell selection. Science (New York, N.Y.) 2014, 345: 1058-62. PMID: 25170154, PMCID: PMC4519234, DOI: 10.1126/science.1257861.
  • 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. Development of autoimmune diabetes in the absence of detectable IL-17A in a CD8-driven virally induced model. Journal Of Immunology (Baltimore, Md. : 1950) 2011, 187: 2915-22. PMID: 21832162, PMCID: PMC3169711, DOI: 10.4049/jimmunol.1000180.
  • Oct-1 regulates IL-17 expression by directing interchromosomal associations in conjunction with CTCF in T cells.Kim LK, Esplugues E, Zorca CE, Parisi F, Kluger Y, Kim TH, Galjart NJ, Flavell RA. Oct-1 regulates IL-17 expression by directing interchromosomal associations in conjunction with CTCF in T cells. Molecular Cell 2014, 54: 56-66. PMID: 24613343, PMCID: PMC4058095, DOI: 10.1016/j.molcel.2014.02.004.
  • Bcl6 expression specifies the T follicular helper cell program in vivo.Liu X, Yan X, Zhong B, Nurieva RI, Wang A, Wang X, Martin-Orozco N, Wang Y, Chang SH, Esplugues E, Flavell RA, Tian Q, Dong C. Bcl6 expression specifies the T follicular helper cell program in vivo. The Journal Of Experimental Medicine 2012, 209: 1841-52, S1-24. PMID: 22987803, PMCID: PMC3457730, DOI: 10.1084/jem.20120219.
  • Control of TH17 cells occurs in the small intestine.Esplugues E, Huber S, Gagliani N, Hauser AE, Town T, Wan YY, O'Connor W, Rongvaux A, Van Rooijen N, Haberman AM, Iwakura Y, Kuchroo VK, Kolls JK, Bluestone JA, Herold KC, Flavell RA. Control of TH17 cells occurs in the small intestine. Nature 2011, 475: 514-8. PMID: 21765430, PMCID: PMC3148838, DOI: 10.1038/nature10228.
  • 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. miR-33a/b contribute to the regulation of fatty acid metabolism and insulin signaling. Proceedings Of The National Academy Of Sciences Of The United States Of America 2011, 108: 9232-7. PMID: 21576456, PMCID: PMC3107310, DOI: 10.1073/pnas.1102281108.
  • 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, Huber FJ, Chaudhry A, Kamanaka M, Kobayashi Y, Booth CJ, Rudensky AY, Roncarolo MG, Battaglia M, Flavell RA. Th17 cells express interleukin-10 receptor and are controlled by Foxp3⁻ and Foxp3+ regulatory CD4+ T cells in an interleukin-10-dependent manner. Immunity 2011, 34: 554-65. PMID: 21511184, PMCID: PMC3113617, DOI: 10.1016/j.immuni.2011.01.020.
  • 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. Induction of tumor NK-cell immunity by anti-CD69 antibody therapy. Blood 2005, 105: 4399-406. PMID: 15692061, DOI: 10.1182/blood-2004-10-3854.
  • 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. CD69 downregulates autoimmune reactivity through active transforming growth factor-beta production in collagen-induced arthritis. The Journal Of Clinical Investigation 2003, 112: 872-82. PMID: 12975472, PMCID: PMC193672, DOI: 10.1172/JCI19112.
  • 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. Enhanced antitumor immunity in mice deficient in CD69. The Journal Of Experimental Medicine 2003, 197: 1093-106. PMID: 12732655, PMCID: PMC2193974, DOI: 10.1084/jem.20021337.
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