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).
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. J Exp Med. 2012 Sep 24;209(10):1841-52
Effector CD4+ T cell expression signatures and immune-mediated disease associated genes. Zhang W, Ferguson J, Ng SM, Hui K, Goh G, Lin A, Esplugues E, Flavell RA, Abraham C, Zhao H, Cho JH PLoS One. 2012 June 8.
Enhanced anti-serpin antibody activity inhibits autoimmune inflammation in type-1 diabetes. Czyzyk J, Henegariu O, Preston-Hurlburt P, Badzizhar R, Fedorchuk C, Esplugues E, Bottomly K, Gorus FK, Herold K, Flavell RA J Immunol. 2012 June 15; 188(12):6319-27
Mir-33 regulates cell proliferation and cell cycle progression. Cirera-Salinas D, Pauta M, Allen RM, Salerno AG, Ramírez CM, Chamorro-Jorganes A, Wanschel AC, Lasuncion MA, Morales-Ruiz M, Suarez Y, Baldan A, Esplugues E, Fernández-Hernando C. Cell Cycle. 2012 Mar 1;11(5)
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: 18
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
Prof. Carlos Fernandez-Hernando, Division of Cardiology, (NYU), USA
Prof. Richard Flavell, Immunobiology, Yale University, New Haven, USA
Prof. Anja Hauser, Immunodynamics, DRFZ, Berlin