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1-7 of 7
Juliana Idoyaga
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Journal Articles
Marie-Luise Berres, Karen Phaik Har Lim, Tricia Peters, Jeremy Price, Hitoshi Takizawa, Hélène Salmon, Juliana Idoyaga, Albert Ruzo, Philip J. Lupo, M. John Hicks, Albert Shih, Stephen J. Simko, Harshal Abhyankar, Rikhia Chakraborty, Marylene Leboeuf, Monique Beltrão, Sérgio A. Lira, Kenneth M. Heym, Björn E. Clausen, Venetia Bigley, Matthew Collin, Markus G. Manz, Kenneth McClain, Miriam Merad, Carl E. Allen
Journal:
Journal of Experimental Medicine
Journal of Experimental Medicine (2015) 212 (2): 281.
Published: 02 February 2015
Journal Articles
Marie-Luise Berres, Karen Phaik Har Lim, Tricia Peters, Jeremy Price, Hitoshi Takizawa, Hélène Salmon, Juliana Idoyaga, Albert Ruzo, Philip J. Lupo, M. John Hicks, Albert Shih, Stephen J. Simko, Harshal Abhyankar, Rikhia Chakraborty, Marylene Leboeuf, Monique Beltrão, Sérgio A. Lira, Kenneth M. Heym, Björn E. Clausen, Venetia Bigley, Matthew Collin, Markus G. Manz, Kenneth McClain, Miriam Merad, Carl E. Allen
Journal:
Journal of Experimental Medicine
Journal of Experimental Medicine (2014) 211 (4): 669–683.
Published: 17 March 2014
Abstract
Langerhans cell histiocytosis (LCH) is a clonal disorder with elusive etiology, characterized by the accumulation of CD207 + dendritic cells (DCs) in inflammatory lesions. Recurrent BRAF-V600E mutations have been reported in LCH. In this study, lesions from 100 patients were genotyped, and 64% carried the BRAF-V600E mutation within infiltrating CD207 + DCs. BRAF-V600E expression in tissue DCs did not define specific clinical risk groups but was associated with increased risk of recurrence. Strikingly, we found that patients with active, high-risk LCH also carried BRAF-V600E in circulating CD11c + and CD14 + fractions and in bone marrow (BM) CD34 + hematopoietic cell progenitors, whereas the mutation was restricted to lesional CD207 + DC in low-risk LCH patients. Importantly, BRAF-V600E expression in DCs was sufficient to drive LCH-like disease in mice. Consistent with our findings in humans, expression of BRAF-V600E in BM DC progenitors recapitulated many features of the human high-risk LCH, whereas BRAF-V600E expression in differentiated DCs more closely resembled low-risk LCH. We therefore propose classification of LCH as a myeloid neoplasia and hypothesize that high-risk LCH arises from somatic mutation of a hematopoietic progenitor, whereas low-risk disease arises from somatic mutation of tissue-restricted precursor DCs.
Includes: Supplementary data
Journal Articles
Matthew M. Meredith, Kang Liu, Alice O. Kamphorst, Juliana Idoyaga, Arito Yamane, Pierre Guermonprez, Suzannah Rihn, Kai-Hui Yao, Israel T. Silva, Thiago Y. Oliveira, Dimitris Skokos, Rafael Casellas, Michel C. Nussenzweig
Journal:
Journal of Experimental Medicine
Journal of Experimental Medicine (2012) 209 (9): 1583–1593.
Published: 30 July 2012
Abstract
Classical dendritic cells (cDCs) process and present antigens to T cells. Under steady-state conditions, antigen presentation by cDCs induces tolerance. In contrast, during infection or inflammation, cDCs become activated, express higher levels of cell surface MHC molecules, and induce strong adaptive immune responses. We recently identified a cDC-restricted zinc finger transcription factor, zDC (also known as Zbtb46 or Btbd4), that is not expressed by other immune cell populations, including plasmacytoid DCs, monocytes, or macrophages. We define the zDC consensus DNA binding motif and the genes regulated by zDC using chromatin immunoprecipitation and deep sequencing. By deleting zDC from the mouse genome, we show that zDC is primarily a negative regulator of cDC gene expression. zDC deficiency alters the cDC subset composition in the spleen in favor of CD8 + DCs, up-regulates activation pathways in steady-state cDCs, including elevated MHC II expression, and enhances cDC production of vascular endothelial growth factor leading to increased vascularization of skin-draining lymph nodes. Consistent with these observations, zDC protein expression is rapidly down-regulated after TLR stimulation. Thus, zDC is a TLR-responsive, cDC-specific transcriptional repressor that is in part responsible for preventing cDC maturation in the steady state.
Includes: Supplementary data
Journal Articles
Matthew M. Meredith, Kang Liu, Guillaume Darrasse-Jeze, Alice O. Kamphorst, Heidi A. Schreiber, Pierre Guermonprez, Juliana Idoyaga, Cheolho Cheong, Kai-Hui Yao, Rachel E. Niec, Michel C. Nussenzweig
Journal:
Journal of Experimental Medicine
Journal of Experimental Medicine (2012) 209 (6): 1153–1165.
Published: 21 May 2012
Abstract
Classical dendritic cells (cDCs), monocytes, and plasmacytoid DCs (pDCs) arise from a common bone marrow precursor (macrophage and DC progenitors [MDPs]) and express many of the same surface markers, including CD11c. We describe a previously uncharacterized zinc finger transcription factor, zDC (Zbtb46, Btbd4), which is specifically expressed by cDCs and committed cDC precursors but not by monocytes, pDCs, or other immune cell populations. We inserted diphtheria toxin (DT) receptor (DTR) cDNA into the 3′ UTR of the zDC locus to serve as an indicator of zDC expression and as a means to specifically deplete cDCs. Mice bearing this knockin express DTR in cDCs but not other immune cell populations, and DT injection into zDC-DTR bone marrow chimeras results in cDC depletion. In contrast to previously characterized CD11c-DTR mice, non-cDCs, including pDCs, monocytes, macrophages, and NK cells, were spared after DT injection in zDC-DTR mice. We compared immune responses to Toxoplasma gondii and MO4 melanoma in DT-treated zDC- and CD11c-DTR mice and found that immunity was only partially impaired in zDC-DTR mice. Our results indicate that CD11c-expressing non-cDCs make significant contributions to initiating immunity to parasites and tumors.
Journal Articles
Fabienne Billiard, Camille Lobry, Guillaume Darrasse-Jèze, Janelle Waite, Xia Liu, Hugo Mouquet, Amanda DaNave, Michelle Tait, Juliana Idoyaga, Marylène Leboeuf, Christos A. Kyratsous, Jacquelynn Burton, Julie Kalter, Apostolos Klinakis, Wen Zhang, Gavin Thurston, Miriam Merad, Ralph M. Steinman, Andrew J. Murphy, George D. Yancopoulos, Iannis Aifantis, Dimitris Skokos
Journal:
Journal of Experimental Medicine
Journal of Experimental Medicine (2012) 209 (5): 1011–1028.
Published: 30 April 2012
Abstract
Delta-like ligand 4 (Dll4)–Notch signaling is essential for T cell development and alternative thymic lineage decisions. How Dll4–Notch signaling affects pro-T cell fate and thymic dendritic cell (tDC) development is unknown. We found that Dll4 pharmacological blockade induces accumulation of tDCs and CD4 + CD25 + FoxP3 + regulatory T cells (T reg cells) in the thymic cortex. Both genetic inactivation models and anti-Dll4 antibody (Ab) treatment promote de novo natural T reg cell expansion by a DC-dependent mechanism that requires major histocompatibility complex II expression on DCs. Anti-Dll4 treatment converts CD4 − CD8 − c-kit + CD44 + CD25 − (DN1) T cell progenitors to immature DCs that induce ex vivo differentiation of naive CD4 + T cells into T reg cells. Induction of these tolerogenic DN1-derived tDCs and the ensuing expansion of T reg cells are Fms-like tyrosine kinase 3 (Flt3) independent, occur in the context of transcriptional up-regulation of PU.1 , Irf-4 , Irf-8 , and CSF-1 , genes critical for DC differentiation, and are abrogated in thymectomized mice. Anti-Dll4 treatment fully prevents type 1 diabetes (T1D) via a T reg cell–mediated mechanism and inhibits CD8 + T cell pancreatic islet infiltration. Furthermore, a single injection of anti-Dll4 Ab reverses established T1D. Disease remission and recurrence are correlated with increased T reg cell numbers in the pancreas-draining lymph nodes. These results identify Dll4–Notch as a novel Flt3-alternative pathway important for regulating tDC-mediated T reg cell homeostasis and autoimmunity.
Journal Articles
M. Paula Longhi, Christine Trumpfheller, Juliana Idoyaga, Marina Caskey, Ines Matos, Courtney Kluger, Andres M. Salazar, Marco Colonna, Ralph M. Steinman
Journal:
Journal of Experimental Medicine
Journal of Experimental Medicine (2009) 206 (7): 1589–1602.
Published: 29 June 2009
Abstract
Relative to several other toll-like receptor (TLR) agonists, we found polyinosinic:polycytidylic acid (poly IC) to be the most effective adjuvant for Th1 CD4 + T cell responses to a dendritic cell (DC)–targeted HIV gag protein vaccine in mice. To identify mechanisms for adjuvant action in the intact animal and the polyclonal T cell repertoire, we found poly IC to be the most effective inducer of type I interferon (IFN), which was produced by DEC-205 + DCs, monocytes, and stromal cells. Antibody blocking or deletion of type I IFN receptor showed that IFN was essential for DC maturation and development of CD4 + immunity. The IFN-AR receptor was directly required for DCs to respond to poly IC. STAT 1 was also essential, in keeping with the type I IFN requirement, but not type II IFN or IL-12 p40. Induction of type I IFN was mda5 dependent, but DCs additionally used TLR3. In bone marrow chimeras, radioresistant and, likely, nonhematopoietic cells were the main source of IFN, but mda5 was required in both marrow–derived and radioresistant host cells for adaptive responses. Therefore, the adjuvant action of poly IC requires a widespread innate type I IFN response that directly links antigen presentation by DCs to adaptive immunity.
Includes: Supplementary data
Journal Articles
Kang Liu, Juliana Idoyaga, Anna Charalambous, Shin-ichiro Fujii, Anthony Bonito, Jose Mordoh, Rosa Wainstok, Xue-Feng Bai, Yang Liu, Ralph M. Steinman
Journal:
Journal of Experimental Medicine
Journal of Experimental Medicine (2005) 202 (11): 1507–1516.
Published: 05 December 2005
Abstract
If irradiated tumor cells could be rendered immunogenic, they would provide a safe, broad, and patient-specific array of antigens for immunotherapies. Prior approaches have emphasized genetic transduction of live tumor cells to express cytokines, costimulators, and surrogate foreign antigens. We asked if immunity could be achieved by delivering irradiated, major histocompatibility complex–negative plasmacytoma cells to maturing mouse dendritic cells (DCs) within lymphoid organs. Tumor cells injected intravenously (i.v.) were captured by splenic DCs, whereas subcutaneous (s.c.) injection led only to weak uptake in lymph node or spleen. The natural killer T (NKT) cells mobilizing glycolipid α -galactosyl ceramide, used to mature splenic DCs, served as an effective adjuvant to induce protective immunity. This adjuvant function was mimicked by a combination of poly IC and agonistic α CD40 antibody. The adjuvant glycolipid had to be coadministered with tumor cells i.v. rather than s.c. Specific resistance was generated both to a plasmacytoma and lymphoma. The resistance afforded by a single vaccination lasted >2 mo and required both CD4 + and CD8 + T cells. Mature tumor capturing DCs stimulated the differentiation of P1A tumor antigen-specific, CD8 + T cells and uniquely transferred tumor resistance to naive mice. Therefore, the access of dying tumor cells to DCs that are maturing to activated NKT cells efficiently induces long-lived adaptive resistance.
Includes: Supplementary data