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1. Identification of environmental factors that promote intestinal inflammation

Author

Sanmarco, Liliana M., Chao, Chun-Cheih, Wang, Yu-Chao, Kenison, Jessica E., Li, Zhaorong, Rone, Joseph M., Rejano-Gordillo, Claudia M., Polonio, Carolina M., Gutierrez-Vazquez, Cristina, Piester, Gavin, Plasencia, Agustin, Li, Lucinda, Giovannoni, Federico, Lee, Hong-Gyun, Faust Akl, Camilo, Wheeler, Michael A., Mascanfroni, Ivan, Jaronen, Merja, Alsuwailm, Moneera, Hewson, Patrick, Yeste, Ada, Andersen, Brian M., Franks, Diana G., Huang, Chien-Jung, Ekwudo, Millicent, Tjon, Emily C., Rothhammer, Veit, Takenaka, Maisa, de Lima, Kalil Alves, Linnerbauer, Mathias, Guo, Lydia, Covacu, Ruxandra, Queva, Hugo, Fonseca-Castro, Pedro Henrique, Bladi, Maha Al, Cox, Laura M., Hodgetts, Kevin J., Hahn, Mark E., Mildner, Alexander, Korzenik, Joshua, Hauser, Russ, Snapper, Scott B., and Quintana, Francisco J.

Published
2022
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2. A cell-based drug delivery platform for treating central nervous system inflammation

Author

Levy, Oren, Rothhammer, Veit, Mascanfroni, Ivan, Tong, Zhixiang, Kuai, Rui, De Biasio, Michael, Wang, Qingping, Majid, Tahir, Perrault, Christelle, Yeste, Ada, Kenison, Jessica E., Safaee, Helia, Musabeyezu, Juliet, Heinelt, Martina, Milton, Yuka, Kuang, Heidi, Lan, Haoyue, Siders, William, Multon, Marie-Christine, Rothblatt, Jonathan, Massadeh, Salam, Alaamery, Manal, Alhasan, Ali H., Quintana, Francisco J., and Karp, Jeffrey M.

Published
2021
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4. Fatal autoimmunity in mice reconstituted with human hematopoietic stem cells encoding defective FOXP3

Author

Goettel, Jeremy A., Biswas, Subhabrata, Lexmond, Willem S., Yeste, Ada, Passerini, Laura, Patel, Bonny, Yang, Siyoung, Sun, Jiusong, Ouahed, Jodie, Shouval, Dror S., McCann, Katelyn J., Horwitz, Bruce H., Mathis, Diane, Milford, Edgar L., Notarangelo, Luigi D., Roncarolo, Maria-Grazia, Fiebiger, Edda, Marasco, Wayne A., Bacchetta, Rosa, Quintana, Francisco J., Pai, Sung-Yun, Klein, Christoph, Muise, Aleixo M., and Snapper, Scott B.

Published
2015
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6. Metabolic control of type 1 regulatory T cell differentiation by AHR and HIF1-α

Author

Mascanfroni, Ivan D., Takenaka, Maisa C., Yeste, Ada, Patel, Bonny, Wu, Yan, Kenison, Jessica E., Siddiqui, Shafiuddin, Basso, Alexandre S., Otterbein, Leo E., Pardoll, Drew M., Pan, Fan, Priel, Avner, Clish, Clary B., Robson, Simon C., and Quintana, Francisco J.

Subjects
T cells -- Physiological aspects -- Genetic aspects -- Research, Gene expression -- Physiological aspects -- Research, Cell differentiation -- Physiological aspects -- Genetic aspects -- Research, Biological sciences, Health
Abstract

Our understanding of the pathways that regulate lymphocyte metabolism, as well as the effects of metabolism and its products on the immune response, is still limited. We report that a metabolic program controlled by the transcription factors hypoxia inducible factor-1α (HIF1-α) and aryl hydrocarbon receptor (AHR) supports the differentiation of type 1 regulatory T cell (Tr1) cells. HIF1-α controls the early metabolic reprograming of Tr1 cells. At later time points, AHR promotes HIF1-α degradation and takes control of Tr1 cell metabolism. Extracellular ATP (eATP) and hypoxia, linked to inflammation, trigger AHR inactivation by HIF1-α and inhibit Tr1 cell differentiation. Conversely, CD39 promotes Tr1 cell differentiation by depleting eATP. CD39 also contributes to Tr1 suppressive activity by generating adenosine in cooperation with CD73 expressed by responder T cells and antigen-presenting cells. These results suggest that HIF1-α and AHR integrate immunological, metabolic and environmental signals to regulate the immune response., T cell activation triggers metabolic changes required to support the adaptive immune response (1-5). Indeed, the differentiation of cytotoxic and interleukin (IL)-17-producing effector T cells (T helper 17 cells; [T.sub.H]17 [...]

Published
2015
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10. Regulation of astrocyte activation by glycolipids drives chronic CNS inflammation

Author

Mayo, Lior, Trauger, Sunia A., Blain, Manon, Nadeau, Meghan, Patel, Bonny, Alvarez, Jorge I., Mascanfroni, Ivan D., Yeste, Ada, Kivisakk, Pia, Kallas, Keith, Ellezam, Benjamin, Bakshi, Rohit, Prat, Alexandre, Antel, Jack P., Weiner, Howard L., and Quintana, Francisco J.

Subjects
Inflammation -- Analysis -- Research, Astrocytes -- Research -- Analysis, Central nervous system -- Research -- Analysis, Biological sciences, Health
Abstract

Astrocytes have complex roles in health and disease, thus it is important to study the pathways that regulate their function. Here we report that lactosylceramide (LacCer) synthesized by β-1,4-galactosyltransferase 6 (B4GALT6) is upregulated in the central nervous system (CNS) of mice during chronic experimental autoimmune encephalomyelitis (EAE), a model of multiple sclerosis (MS). LacCer acts in an autocrine manner to control astrocyte transcriptional programs that promote neurodegeneration. In addition, LacCer in astrocytes controls the recruitment and activation of microglia and CNS-infiltrating monocytes in a non-cell autonomous manner by regulating production of the chemokine CCL2 and granulocyte-macrophage colony-stimulating factor (GM-CSF), respectively. We also detected high B4GALT6 gene expression and LacCer concentrations in CNS MS lesions. Inhibition of LacCer synthesis in mice suppressed local CNS innate immunity and neurodegeneration in EAE and interfered with the activation of human astrocytes in vitro. Thus, B4GALT6 regulates astrocyte activation and is a potential therapeutic target for MS and other neuroinflammatory disorders., Astrocytes are the most abundant cells in the CNS. Under normal conditions, astrocytes modulate synaptic activity and provide nutrients and support for neuronal survival (1-4). In the context of neuroinflammation, [...]

Published
2014
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11. A cell-based drug delivery platform for treating central nervous system inflammation

Author

Harvard University--MIT Division of Health Sciences and Technology, Broad Institute of MIT and Harvard, Levy, Oren, Rothhammer, Veit, Mascanfroni, Ivan, Tong, Zhixiang, Kuai, Rui, De Biasio, Michael, Wang, Qingping, Majid, Tahir, Perrault, Christelle, Yeste, Ada, Kenison, Jessica E., Safaee, Helia, Musabeyezu, Juliet, Heinelt, Martina, Milton, Yuka, Kuang, Heidi, Lan, Haoyue, Siders, William, Multon, Marie-Christine, Rothblatt, Jonathan, Massadeh, Salam, Alaamery, Manal, Alhasan, Ali H., Quintana, Francisco J., Karp, Jeffrey Michael, Harvard University--MIT Division of Health Sciences and Technology, Broad Institute of MIT and Harvard, Levy, Oren, Rothhammer, Veit, Mascanfroni, Ivan, Tong, Zhixiang, Kuai, Rui, De Biasio, Michael, Wang, Qingping, Majid, Tahir, Perrault, Christelle, Yeste, Ada, Kenison, Jessica E., Safaee, Helia, Musabeyezu, Juliet, Heinelt, Martina, Milton, Yuka, Kuang, Heidi, Lan, Haoyue, Siders, William, Multon, Marie-Christine, Rothblatt, Jonathan, Massadeh, Salam, Alaamery, Manal, Alhasan, Ali H., Quintana, Francisco J., and Karp, Jeffrey Michael

Abstract

Mesenchymal stem cells (MSCs) are promising candidates for the development of cell-based drug delivery systems for autoimmune inflammatory diseases, such as multiple sclerosis (MS). Here, we investigated the effect of Ro-31-8425, an ATP-competitive kinase inhibitor, on the therapeutic properties of MSCs. Upon a simple pretreatment procedure, MSCs spontaneously took up and then gradually released significant amounts of Ro-31-8425. Ro-31-8425 (free or released by MSCs) suppressed the proliferation of CD4+ T cells in vitro following polyclonal and antigen-specific stimulation. Systemic administration of Ro-31-8425-loaded MSCs ameliorated the clinical course of experimental autoimmune encephalomyelitis (EAE), a murine model of MS, displaying a stronger suppressive effect on EAE than control MSCs or free Ro-31-8425. Ro-31-8425-MSC administration resulted in sustained levels of Ro-31-8425 in the serum of EAE mice, modulating immune cell trafficking and the autoimmune response during EAE. Collectively, these results identify MSC-based drug delivery as a potential therapeutic strategy for the treatment of autoimmune diseases., National Institutes of Health (Grant HL095722)

Published
2021

13. Secreted IgD Amplifies Humoral T Helper 2 Cell Responses by Binding Basophils via Galectin-9 and CD44

Author

Shan, Meimei, primary, Carrillo, Jorge, additional, Yeste, Ada, additional, Gutzeit, Cindy, additional, Segura-Garzón, Daniel, additional, Walland, A. Cooper, additional, Pybus, Marc, additional, Grasset, Emilie K., additional, Yeiser, John R., additional, Matthews, Dean B., additional, van de Veen, Willem, additional, Comerma, Laura, additional, He, Bing, additional, Boonpiyathad, Tadech, additional, Lee, Haekyung, additional, Blanco, Julià, additional, Osborne, Lisa C., additional, Siracusa, Mark C., additional, Akdis, Mübeccel, additional, Artis, David, additional, Mehandru, Saurabh, additional, Sampson, Hugh A., additional, Berin, M. Cecilia, additional, Chen, Kang, additional, and Cerutti, Andrea, additional

Published
2018
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14. Human Secretory IgM Emerges from Plasma Cells Clonally Related to Gut Memory B Cells and Targets Highly Diverse Commensals

Author

Magri, Giuliana, Comerma, Laura, Pybus, Marc, Sintes, Jordi, Lligé, David, Segura-Garzón, Daniel, Bascones, Sabrina, Yeste, Ada, Grasset, Emilie K., Gutzeit, Cindy, Uzzan, Mathieu, Ramanujam, Meera, van Zelm, Menno C., Albero-González, Raquel, Vazquez, Ivonne, Iglesias, Mar, Serrano, Sergi, Márquez, Lucía, Mercade, Elena, Mehandru, Saurabh, Cerutti, Andrea, Magri, Giuliana, Comerma, Laura, Pybus, Marc, Sintes, Jordi, Lligé, David, Segura-Garzón, Daniel, Bascones, Sabrina, Yeste, Ada, Grasset, Emilie K., Gutzeit, Cindy, Uzzan, Mathieu, Ramanujam, Meera, van Zelm, Menno C., Albero-González, Raquel, Vazquez, Ivonne, Iglesias, Mar, Serrano, Sergi, Márquez, Lucía, Mercade, Elena, Mehandru, Saurabh, and Cerutti, Andrea

Abstract

Secretory immunoglobulin A (SIgA) enhances host-microbiota symbiosis, whereas SIgM remains poorly understood. We found that gut IgM+ plasma cells (PCs) were more abundant in humans than mice and clonally related to a large repertoire of memory IgM+ B cells disseminated throughout the intestine but rare in systemic lymphoid organs. In addition to sharing a gut-specific gene signature with memory IgA+ B cells, memory IgM+ B cells were related to some IgA+ clonotypes and switched to IgA in response to T cell-independent or T cell-dependent signals. These signals induced abundant IgM which, together with SIgM from clonally affiliated PCs, recognized mucus-embedded commensals. Bacteria recognized by human SIgM were dually coated by SIgA and showed increased richness and diversity compared to IgA-only-coated or uncoated bacteria. Thus, SIgM may emerge from pre-existing memory rather than newly activated naive IgM+ B cells and could help SIgA to anchor highly diverse commensal communities to mucus. Magri et al. found that the human gut includes a large memory IgM+ B cell repertoire clonally related to plasma cells mounting SIgM responses against mucus-embedded commensals co-targeted by SIgA. Dually coated bacteria are detected in humans but not mice and show increased diversity and richness compared to SIgA-only-coated or uncoated bacteria.

Published
2017

16. Human Secretory IgM Emerges from Plasma Cells Clonally Related to Gut Memory B Cells and Targets Highly Diverse Commensals

Author

Magri, Giuliana, primary, Comerma, Laura, additional, Pybus, Marc, additional, Sintes, Jordi, additional, Lligé, David, additional, Segura-Garzón, Daniel, additional, Bascones, Sabrina, additional, Yeste, Ada, additional, Grasset, Emilie K., additional, Gutzeit, Cindy, additional, Uzzan, Mathieu, additional, Ramanujam, Meera, additional, van Zelm, Menno C., additional, Albero-González, Raquel, additional, Vazquez, Ivonne, additional, Iglesias, Mar, additional, Serrano, Sergi, additional, Márquez, Lucía, additional, Mercade, Elena, additional, Mehandru, Saurabh, additional, and Cerutti, Andrea, additional

Published
2017
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17. Bilirubin suppresses Th17 immunity in colitis by upregulating CD39

Author

Longhi, Maria Serena, primary, Vuerich, Marta, additional, Kalbasi, Alireza, additional, Kenison, Jessica E., additional, Yeste, Ada, additional, Csizmadia, Eva, additional, Vaughn, Byron, additional, Feldbrugge, Linda, additional, Mitshuhashi, Shuji, additional, Wegiel, Barbara, additional, Otterbein, Leo, additional, Moss, Alan, additional, Quintana, Francisco J., additional, and Robson, Simon C., additional

Published
2017
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18. AHR Activation Is Protective against Colitis Driven by T Cells in Humanized Mice

Author

Goettel, Jeremy A., primary, Gandhi, Roopali, additional, Kenison, Jessica E., additional, Yeste, Ada, additional, Murugaiyan, Gopal, additional, Sambanthamoorthy, Sharmila, additional, Griffith, Alexandra E., additional, Patel, Bonny, additional, Shouval, Dror S., additional, Weiner, Howard L., additional, Snapper, Scott B., additional, and Quintana, Francisco J., additional

Published
2016
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19. Tolerogenic nanoparticles inhibit T cell–mediated autoimmunity through SOCS2

Author

Yeste, Ada, primary, Takenaka, Maisa C., additional, Mascanfroni, Ivan D., additional, Nadeau, Meghan, additional, Kenison, Jessica E., additional, Patel, Bonny, additional, Tukpah, Ann-Marcia, additional, Babon, Jenny Aurielle B., additional, DeNicola, Megan, additional, Kent, Sally C., additional, Pozo, David, additional, and Quintana, Francisco J., additional

Published
2016
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20. Digestion of Chromatin in Apoptotic Cell Microparticles Prevents Autoimmunity

Author

Sisirak, Vanja, primary, Sally, Benjamin, additional, D’Agati, Vivette, additional, Martinez-Ortiz, Wilnelly, additional, Özçakar, Z. Birsin, additional, David, Joseph, additional, Rashidfarrokhi, Ali, additional, Yeste, Ada, additional, Panea, Casandra, additional, Chida, Asiya Seema, additional, Bogunovic, Milena, additional, Ivanov, Ivaylo I., additional, Quintana, Francisco J., additional, Sanz, Inaki, additional, Elkon, Keith B., additional, Tekin, Mustafa, additional, Yalçınkaya, Fatoş, additional, Cardozo, Timothy J., additional, Clancy, Robert M., additional, Buyon, Jill P., additional, and Reizis, Boris, additional

Published
2016
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23. Melatonin Contributes to the Seasonality of Multiple Sclerosis Relapses

Author

Farez, Mauricio F., primary, Mascanfroni, Ivan D., additional, Méndez-Huergo, Santiago P., additional, Yeste, Ada, additional, Murugaiyan, Gopal, additional, Garo, Lucien P., additional, Balbuena Aguirre, María E., additional, Patel, Bonny, additional, Ysrraelit, María C., additional, Zhu, Chen, additional, Kuchroo, Vijay K., additional, Rabinovich, Gabriel A., additional, Quintana, Francisco J., additional, and Correale, Jorge, additional

Published
2015
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24. B4GALT6 regulates astrocyte activation during CNS inflammation (INM8P.360)

Author

Mayo, Lior, primary, Trauger, Sunia, additional, Blain, Manon, additional, Mascanfroni, Ivan, additional, Kivisäkk, Pia, additional, Yeste, Ada, additional, Bakshi, Rohit, additional, Alvarez, Jorge Iván, additional, Prat, Alexandre, additional, Antel, Jack, additional, Weiner, Howard, additional, and Quintana, Francisco, additional

Published
2015
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25. IL-27 acts on DCs to suppress CNS autoimmunity by inducing CD39 expression

Author

Mascanfroni, Ivan, primary, Yeste, Ada, additional, Vieira, Silvio, additional, Burns, Evans, additional, Patel, Bonny, additional, Sloma, Ido, additional, Wu, Yan, additional, Mayo, Lior, additional, Ben-hamo, Rotem, additional, Efroni, Sol, additional, Kuchroo, Vijay, additional, Robson, Simon, additional, and Quintana, Francisco, additional

Published
2014
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26. IL-21 induces IL-22 production in CD4+ T cells

Author

Yeste, Ada, primary, Mascanfroni, Ivan D., additional, Nadeau, Meghan, additional, Burns, Evan J., additional, Tukpah, Ann-Marcia, additional, Santiago, Andrezza, additional, Wu, Chuan, additional, Patel, Bonny, additional, Kumar, Deepak, additional, and Quintana, Francisco J, additional

Published
2014
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28. IL-27 acts on DCs to suppress the T cell response and autoimmunity by inducing expression of the immunoregulatory molecule CD39

Author

Mascanfroni, Ivan D, primary, Yeste, Ada, additional, Vieira, Silvio M, additional, Burns, Evan J, additional, Patel, Bonny, additional, Sloma, Ido, additional, Wu, Yan, additional, Mayo, Lior, additional, Ben-Hamo, Rotem, additional, Efroni, Sol, additional, Kuchroo, Vijay K, additional, Robson, Simon C, additional, and Quintana, Francisco J, additional

Published
2013
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33. Aiolos promotes TH17 differentiation by directly silencing Il2 expression

Author

Quintana, Francisco J, primary, Jin, Hulin, additional, Burns, Evan J, additional, Nadeau, Meghan, additional, Yeste, Ada, additional, Kumar, Deepak, additional, Rangachari, Manu, additional, Zhu, Chen, additional, Xiao, Sheng, additional, Seavitt, John, additional, Georgopoulos, Katia, additional, and Kuchroo, Vijay K, additional

Published
2012
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35. Epitope spreading as an early pathogenic event in pediatric multiple sclerosis.

Author

Quintana, Francisco J, Patel, Bonny, Yeste, Ada, Nyirenda, Mukanthu, Kenison, Jessica, Rahbari, Roya, Fetco, Dumitru, Hussain, Mohammad, O'Mahony, Julia, Magalhaes, Sandra, McGowan, Melissa, Johnson, Trina, Rajasekharan, Sathy, Narayanan, Sridar, Arnold, Douglas L, Weiner, Howard L, Banwell, Brenda, Bar-Or, Amit, and Canadian Pediatric Demyelinating Disease Network

Published
2014
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36. Aiolos promotes TH17 differentiation by directly silencing Il2 expression.

Author

Quintana, Francisco J, Jin, Hulin, Burns, Evan J, Nadeau, Meghan, Yeste, Ada, Kumar, Deepak, Rangachari, Manu, Zhu, Chen, Xiao, Sheng, Seavitt, John, Georgopoulos, Katia, and Kuchroo, Vijay K

Subjects
T helper cells, CELL differentiation, INTERLEUKIN-2, IMMUNOLOGY of inflammation, TRANSCRIPTION factors, AUTOIMMUNITY, LOCUS (Genetics), GENE silencing
Abstract

CD4+ interleukin 17 (IL-17)-producing helper T cells (TH17 cells) are instrumental in the immune response to pathogens. However, an overactive TH17 response results in tissue inflammation and autoimmunity, and therefore it is important to identify the molecular mechanisms that control the development of TH17 cells. IL-2 suppresses such development, but how IL-2 production is actively suppressed during TH7 differentiation is not understood. Here we report that under TH17-polarizing conditions, the transcription factors STAT3 and AhR upregulated the expression of Aiolos, a member of the Ikaros family of transcription factors. Using Aiolos-deficient mice, we demonstrated that Aiolos silenced the Il2 locus, promoting TH17 differentiation in vitro and in vivo. Thus, we have identified a module in the transcriptional program of TH17 cells that actively limits IL-2 production and promotes their differentiation. [ABSTRACT FROM AUTHOR]

Published
2012
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37. Chi3l3 induces oligodendrogenesis in an experimental model of autoimmune neuroinflammation

Author

Starossom, Sarah C., Garcia, Juliana Campo, Woelfle, Tim, Romero-Suarez, Silvina, Olah, Marta, Watanabe, Fumihiro, Cao, Li, Yeste, Ada, Tukker, John J., Quintana, Francisco J., Imitola, Jaime, Witzel, Franziska, Schmitz, Dietmar, Morkel, Markus, Paul, Friedemann, Infante-Duarte, Carmen, and Khoury, Samia J.

Subjects
oligodendrogenesis, multiple sclerosis, 600 Technik, Medizin, angewandte Wissenschaften::610 Medizin und Gesundheit::610 Medizin und Gesundheit, 3. Good health
Abstract

In demyelinating diseases including multiple sclerosis (MS), neural stem cells (NSCs) can replace damaged oligodendrocytes if the local microenvironment supports the required differentiation process. Although chitinase-like proteins (CLPs) form part of this microenvironment, their function in this differentiation process is unknown. Here, we demonstrate that murine Chitinase 3-like-3 (Chi3l3/Ym1), human Chi3L1 and Chit1 induce oligoden-drogenesis. In mice, Chi3l3 is highly expressed in the subventricular zone, a stem cell niche of the adult brain, and in inflammatory brain lesions during experimental autoimmune encephalomyelitis (EAE). We find that silencing Chi3l3 increases severity of EAE. We present evidence that in NSCs Chi3l3 activates the epidermal growth factor receptor (EGFR), thereby inducing Pyk2-and Erk1/2- dependent expression of a pro-oligodendrogenic transcription factor signature. Our results implicate CLP-EGFR-Pyk2-MEK-ERK as a key intrinsic pathway controlling oligodendrogenesis.

39. Serum lipid antibodies are associated with cerebral tissue damage in multiple sclerosis.

Author

Bakshi R, Yeste A, Patel B, Tauhid S, Tummala S, Rahbari R, Chu R, Regev K, Kivisäkk P, Weiner HL, and Quintana FJ

Abstract

Objective: To determine whether peripheral immune responses as measured by serum antigen arrays are linked to cerebral MRI measures of disease severity in multiple sclerosis (MS)., Methods: In this cross-sectional study, serum samples were obtained from patients with relapsing-remitting MS (n = 21) and assayed using antigen arrays that contained 420 antigens including CNS-related autoantigens, lipids, and heat shock proteins. Normalized compartment-specific global brain volumes were obtained from 3-tesla MRI as surrogates of atrophy, including gray matter fraction (GMF), white matter fraction (WMF), and total brain parenchymal fraction (BPF). Total brain T2 hyperintense lesion volume (T2LV) was quantified from fluid-attenuated inversion recovery images., Results: We found serum antibody patterns uniquely correlated with BPF, GMF, WMF, and T2LV. Furthermore, we identified immune signatures linked to MRI markers of neurodegeneration (BPF, GMF, WMF) that differentiated those linked to T2LV. Each MRI measure was correlated with a specific set of antibodies. Strikingly, immunoglobulin G (IgG) antibodies to lipids were linked to brain MRI measures. Based on the association between IgG antibody reactivity and each unique MRI measure, we developed a lipid index. This comprised the reactivity directed against all of the lipids associated with each specific MRI measure. We validated these findings in an additional independent set of patients with MS (n = 14) and detected a similar trend for the correlations between BPF, GMF, and T2LV vs their respective lipid indexes., Conclusions: We propose serum antibody repertoires that are associated with MRI measures of cerebral MS involvement. Such antibodies may serve as biomarkers for monitoring disease pathology and progression.

Published
2016
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