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42 results on '"Toribio, Maria L."'

1. The immunopathological landscape of human pre-TCRα deficiency: From rare to common variants

Author

Materna, Marie, primary, Delmonte, Ottavia M., additional, Bosticardo, Marita, additional, Momenilandi, Mana, additional, Conrey, Peyton E., additional, Charmeteau-De Muylder, Bénédicte, additional, Bravetti, Clotilde, additional, Bellworthy, Rebecca, additional, Cederholm, Axel, additional, Staels, Frederik, additional, Ganoza, Christian A., additional, Darko, Samuel, additional, Sayed, Samir, additional, Le Floc’h, Corentin, additional, Ogishi, Masato, additional, Rinchai, Darawan, additional, Guenoun, Andrea, additional, Bolze, Alexandre, additional, Khan, Taushif, additional, Gervais, Adrian, additional, Krüger, Renate, additional, Völler, Mirjam, additional, Palterer, Boaz, additional, Sadeghi-Shabestari, Mahnaz, additional, Langlois de Septenville, Anne, additional, Schramm, Chaim A., additional, Shah, Sanjana, additional, Tello-Cajiao, John J., additional, Pala, Francesca, additional, Amini, Kayla, additional, Campos, Jose S., additional, Lima, Noemia Santana, additional, Eriksson, Daniel, additional, Lévy, Romain, additional, Seeleuthner, Yoann, additional, Jyonouchi, Soma, additional, Ata, Manar, additional, Al Ali, Fatima, additional, Deswarte, Caroline, additional, Pereira, Anaïs, additional, Mégret, Jérôme, additional, Le Voyer, Tom, additional, Bastard, Paul, additional, Berteloot, Laureline, additional, Dussiot, Michaël, additional, Vladikine, Natasha, additional, Cardenas, Paula P., additional, Jouanguy, Emmanuelle, additional, Alqahtani, Mashael, additional, Hasan, Amal, additional, Thanaraj, Thangavel Alphonse, additional, Rosain, Jérémie, additional, Al Qureshah, Fahd, additional, Sabato, Vito, additional, Alyanakian, Marie Alexandra, additional, Leruez-Ville, Marianne, additional, Rozenberg, Flore, additional, Haddad, Elie, additional, Regueiro, Jose R., additional, Toribio, Maria L., additional, Kelsen, Judith R., additional, Salehi, Mansoor, additional, Nasiri, Shahram, additional, Torabizadeh, Mehdi, additional, Rokni-Zadeh, Hassan, additional, Changi-Ashtiani, Majid, additional, Vatandoost, Nasimeh, additional, Moravej, Hossein, additional, Akrami, Seyed Mohammad, additional, Mazloomrezaei, Mohsen, additional, Cobat, Aurélie, additional, Meyts, Isabelle, additional, Toyofuku, Etsushi, additional, Nishimura, Madoka, additional, Moriya, Kunihiko, additional, Mizukami, Tomoyuki, additional, Imai, Kohsuke, additional, Abel, Laurent, additional, Malissen, Bernard, additional, Al-Mulla, Fahd, additional, Alkuraya, Fowzan Sami, additional, Parvaneh, Nima, additional, von Bernuth, Horst, additional, Beetz, Christian, additional, Davi, Frédéric, additional, Douek, Daniel C., additional, Cheynier, Rémi, additional, Langlais, David, additional, Landegren, Nils, additional, Marr, Nico, additional, Morio, Tomohiro, additional, Shahrooei, Mohammad, additional, Schrijvers, Rik, additional, Henrickson, Sarah E., additional, Luche, Hervé, additional, Notarangelo, Luigi D., additional, Casanova, Jean-Laurent, additional, and Béziat, Vivien, additional

Published
2024
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3. Glutathione overproduction mediates lymphoma initiating cells survival and has a sex-dependent effect on lymphomagenesis

Author

Campanero, Miguel R., primary, H-Alcántara, Alberto, additional, Kourani, Omar, additional, Martínez-Núñez, Patricia, additional, Herranz-Martín, Estela, additional, Fuentes, Patricia, additional, Toribio, Maria L., additional, Marcos-Jiménez, Ana, additional, Muñoz-Calleja, Cecilia, additional, and Iglesias, Teresa, additional

Published
2024
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4. T Lymphoid Differentiation in Human Bone Marrow

Author

Klein, Florian, Feldhahn, Niklas, Lee, Sanggyu, Wang, Hui, Ciuffi, Fiammetta, von Elstermann, Mirko, Toribio, María L., Sauer, Heinrich, Wartenberg, Maria, Barath, Varun Singh, Krönke, Martin, Wernet, Peter, Rowley, Janet D., and Müschen, Markus

Published
2003

6. The NOTCH1/CD44 axis drives pathogenesis in a T cell acute lymphoblastic leukemia model

Author

Garcia-Peydro, Marina, Fuentes, Patricia, Mosquera, Marta, Garcia-Leon, Maria J., Alcain, Juan, Rodriguez, Antonio, Miguel, Purification Garcia de, Menendez, Pablo, Weijer, Kees, Spits, Hergen, Scadden, David T., Cuesta-Mateos, Carlos, Munoz-Calleja, Cecilia, Sanchez-Madrid, Francisco, and Toribio, MarIa L.

Subjects
Gene expression -- Research, Acute lymphocytic leukemia -- Analysis -- Health aspects -- Genetic aspects -- Research, Health care industry
Abstract

NOTCH1 is a prevalent signaling pathway in T cell acute lymphoblastic leukemia (T-ALL), but crucial NOTCH1 downstream signals and target genes contributing to T-ALL pathogenesis cannot be retrospectively analyzed in patients and thus remain ill defined. This information is clinically relevant, as initiating lesions that lead to cell transformation and leukemia-initiating cell (LIC) activity are promising therapeutic targets against the major hurdle of T-ALL relapse. Here, we describe the generation in vivo of a human T cell leukemia that recapitulates T-ALL in patients, which arises de novo in immunodeficient mice reconstituted with human hematopoietic progenitors ectopically expressing active NOTCH1. This T-ALL model allowed us to identify CD44 as a direct NOTCH1 transcriptional target and to recognize CD44 overexpression as an early hallmark of preleukemic cells that engraft the BM and finally develop a clonal transplantable T-ALL that infiltrates lymphoid organs and brain. Notably, CD44 is shown to support crucial BM niche interactions necessary for LIC activity of human T-ALL xenografts and disease progression, highlighting the importance of the NOTCH1/CD44 axis in T-ALL pathogenesis. The observed therapeutic benefit of anti-CD44 antibody administration in xenotransplanted mice holds great promise for therapeutic purposes against T-ALL relapse., Introduction T cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematological malignancy characterized by BM infiltration with immature lymphoblasts derived from transformed T cell precursors (1). A common cause of [...]

Published
2018
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10. Efficient preclinical treatment of cortical T cell acute lymphoblastic leukemia with T lymphocytes secreting anti-CD1a T cell engagers

Author

Jiménez-Reinoso, Anaïs, primary, Tirado, Néstor, additional, Martinez-Moreno, Alba, additional, Díaz, Víctor M, additional, García-Peydró, Marina, additional, Hangiu, Oana, additional, Díez-Alonso, Laura, additional, Albitre, Ángela, additional, Penela, Petronila, additional, Toribio, Maria L, additional, Menéndez, Pablo, additional, Álvarez-Vallina, Luis, additional, and Sánchez Martínez, Diego, additional

Published
2022
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14. ICAP‐1 loss impairs CD8 + thymocyte development and leads to reduced marginal zone B cells in mice

Author

Sevilla‐Movilla, Silvia, primary, Fuentes, Patricia, additional, Rodríguez‐García, Yaiza, additional, Arellano‐Sánchez, Nohemi, additional, Krenn, Peter W., additional, de Val, Soledad Isern, additional, Montero‐Herradón, Sara, additional, García‐Ceca, Javier, additional, Burdiel‐Herencia, Valeria, additional, Gardeta, Sofía R., additional, Aguilera‐Montilla, Noemí, additional, Barrio‐Alonso, Celia, additional, Crainiciuc, Georgiana, additional, Bouvard, Daniel, additional, García‐Pardo, Angeles, additional, Zapata, Agustin G., additional, Hidalgo, Andrés, additional, Fässler, Reinhard, additional, Carrasco, Yolanda R., additional, Toribio, Maria L., additional, and Teixidó, Joaquin, additional

Published
2022
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17. From the Developmental Expression of γδ T Cell Receptors to the Implications in the Acquisition of Tolerance

Author

Marinez-A., C., Alonso, J. M., Barcena, Alicia, Aparicio, P., Toribio, Maria L., Compans, R. W., editor, Cooper, M., editor, Koprowski, H., editor, McConnell, I., editor, Melchers, F., editor, Nussenzweig, V., editor, Oldstone, M., editor, Olsnes, S., editor, Potter, M., editor, Saedler, H., editor, Vogt, P. K., editor, Wagner, H., editor, Wilson, I., editor, Pfeffer, Klaus, editor, Heeg, Klaus, editor, Wagner, Hermann, editor, and Riethmüller, Gert, editor

Published
1991
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19. CD3G or CD3D Knockdown in Mature, but Not Immature, T Lymphocytes Similarly Cripples the Human TCRαβ Complex

Author

Garcillán, Beatriz, primary, Fuentes, Patricia, additional, Marin, Ana V., additional, Megino, Rebeca F., additional, Chacon-Arguedas, Daniel, additional, Mazariegos, Marina S., additional, Jiménez-Reinoso, Anaïs, additional, Muñoz-Ruiz, Miguel, additional, Laborda, Raquel G., additional, Cárdenas, Paula P., additional, Fernández-Malavé, Edgar, additional, Toribio, Maria L., additional, and Regueiro, José R., additional

Published
2021
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20. Toward Sézary Syndrome immunotherapy

Author

Marin, Ana V., primary, Megino, Rebeca F., additional, Viñuela, Marcos, additional, Popova, Olga, additional, Real-Arevalo, Irene, additional, Sanchez-Majano, Jose L., additional, Ortiz-Romero, Pablo L., additional, Castro-Panete, Maria J., additional, Mancebo, Esther, additional, Talayero, Paloma, additional, Paz-Artal, Estela, additional, Paciello, Maria L., additional, Martinez-Lopez, Joaquin, additional, Subiza, Jose L., additional, Reche, Pedro A., additional, Lopez-Bigas, Nuria, additional, Marcilla, Miguel, additional, Paradela, Alberto, additional, Moral, Manuel Gomez del, additional, Martinez-Naves, Eduardo, additional, Serrano, Alvaro, additional, Marina-Zarate, Ester, additional, Ramiro, Almudena R., additional, Engel, Pablo, additional, Dominguez, Mercedes, additional, Moreno, Inmaculada, additional, Cortegano, Isabel, additional, de Andres, Belen, additional, Gaspar, Maria L., additional, Garcia-Peydro, Marina, additional, Balas, Antonio, additional, Moreno, Miguel A., additional, Alenda, Raquel, additional, Vicario, Jose L., additional, Luescher, Immanuel F., additional, Toribio, Maria L., additional, Alarcon, Balbino, additional, and Regueiro, Jose R., additional

Published
2021
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21. ICAP‐1 loss impairs CD8+ thymocyte development and leads to reduced marginal zone B cells in mice.

Author

Sevilla‐Movilla, Silvia, Fuentes, Patricia, Rodríguez‐García, Yaiza, Arellano‐Sánchez, Nohemi, Krenn, Peter W., de Val, Soledad Isern, Montero‐Herradón, Sara, García‐Ceca, Javier, Burdiel‐Herencia, Valeria, Gardeta, Sofía R., Aguilera‐Montilla, Noemí, Barrio‐Alonso, Celia, Crainiciuc, Georgiana, Bouvard, Daniel, García‐Pardo, Angeles, Zapata, Agustin G., Hidalgo, Andrés, Fässler, Reinhard, Carrasco, Yolanda R., and Toribio, Maria L.

Subjects
B cells, CELL physiology, CELL adhesion, TRANSCRIPTION factors, THYMOCYTES
Abstract

ICAP‐1 regulates β1‐integrin activation and cell adhesion. Here, we used ICAP‐1‐null mice to study ICAP‐1 potential involvement during immune cell development and function. Integrin α4β1‐dependent adhesion was comparable between ICAP‐1‐null and control thymocytes, but lack of ICAP‐1 caused a defective single‐positive (SP) CD8+ cell generation, thus, unveiling an ICAP‐1 involvement in SP thymocyte development. ICAP‐1 bears a nuclear localization signal and we found it displayed a strong nuclear distribution in thymocytes. Interestingly, there was a direct correlation between the lack of ICAP‐1 and reduced levels in SP CD8+ thymocytes of Runx3, a transcription factor required for CD8+ thymocyte generation. In the spleen, ICAP‐1 was found evenly distributed between cytoplasm and nuclear fractions, and ICAP‐1–/– spleen T and B cells displayed upregulation of α4β1‐mediated adhesion, indicating that ICAP‐1 negatively controls their attachment. Furthermore, CD3+‐ and CD19+‐selected spleen cells from ICAP‐1‐null mice showed reduced proliferation in response to T‐ and B‐cell stimuli, respectively. Finally, loss of ICAP‐1 caused a remarkable decrease in marginal zone B‐ cell frequencies and a moderate increase in follicular B cells. Together, these data unravel an ICAP‐1 involvement in the generation of SP CD8+ thymocytes and in the control of marginal zone B‐cell numbers. [ABSTRACT FROM AUTHOR]

Published
2022
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24. Downregulation of Glutamine Synthetase, not glutaminolysis, is responsible for glutamine addiction in Notch1‐driven acute lymphoblastic leukemia

Author

Nguyen, Tra Ly, primary, Nokin, Marie‐Julie, additional, Terés, Silvia, additional, Tomé, Mercedes, additional, Bodineau, Clément, additional, Galmar, Oriane, additional, Pasquet, Jean‐Max, additional, Rousseau, Benoit, additional, Liempd, Sebastian, additional, Falcon‐Perez, Juan Manuel, additional, Richard, Elodie, additional, Muzotte, Elodie, additional, Rezvani, Hamid‐Reza, additional, Priault, Muriel, additional, Bouchecareilh, Marion, additional, Redonnet‐Vernhet, Isabelle, additional, Calvo, Julien, additional, Uzan, Benjamin, additional, Pflumio, Françoise, additional, Fuentes, Patricia, additional, Toribio, Maria L., additional, Khatib, Abdel‐Majid, additional, Soubeyran, Pierre, additional, Murdoch, Piedad del Socorro, additional, and Durán, Raúl V., additional

Published
2021
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25. Therapeutic potential of an anti-CCR9 mAb evidenced in xenografts of human CCR9+ tumors.

Author

Santamaria, Silvia, Delgado, Marisa, Botas, Marta, Castellano, Eva, Corraliza-Gorjon, Isabel, Lafuente, Paloma, Muñoz-Calleja, Cecilia, Toribio, Maria L., Kremer, Leonor, and Garcia-Sanz, Jose A.

Subjects
CHEMOKINE receptors, LYMPHOBLASTIC leukemia, XENOGRAFTS, ACUTE leukemia, TUMOR treatment, PANCREATIC tumors
Abstract

Relapsed or refractory T acute lymphoblastic leukemia (T-ALL) still carries poor prognosis. Aiming to improve outcomes, the therapeutic potential of an anti-CCR9 monoclonal antibody (mAb 92R), targeting the human chemokinereceptor CCR9 is analyzed on orthotopic xenotransplants. 92R mAb treatment of mice carrying human CCR9+ T-ALL cell lines or primary T cell leukemias inhibits tumor growth and increases survival. The therapeutic effects of 92R are specific and synergize with chemotherapeutic agents increasing survival. Furthermore, 92R decreases size of non-hematopoietic tumors with a forced CCR9 expression and of solid tumors generated by the pancreatic adenocarcinoma cell line AsPC-1. In addition, a humanized version of 92R mAb (Srb1) is also able to inhibit growth of CCR9+ T-ALL tumor cells in vivo, increasing survival 2.66-fold. Finally, 92R mAb prevents liver accumulation of infiltrates and reduces tumor cell numbers in already formed infiltrates. Thus, the humanized version of 92R mAb (Srb1), displays therapeutic potential for CCR9+ tumor treatment and might represent one of the first therapeutic antibodies for precision medicine on T-ALL patients. [ABSTRACT FROM AUTHOR]

Published
2022
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33. Developmental regulation of apical endocytosis controls epithelial patterning in vertebrate tubular organs

Author

Rodríguez-Fraticelli, Alejo E., primary, Bagwell, Jennifer, additional, Bosch-Fortea, Minerva, additional, Boncompain, Gaelle, additional, Reglero-Real, Natalia, additional, García-León, Maria J., additional, Andrés, Germán, additional, Toribio, Maria L., additional, Alonso, Miguel A., additional, Millán, Jaime, additional, Perez, Franck, additional, Bagnat, Michel, additional, and Martín-Belmonte, Fernando, additional

Published
2015
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36. Oncogenic IL7R gain-of-function mutations in childhood T-cell acute lymphoblastic leukemia

Author

Zenatti, Priscila P, primary, Ribeiro, Daniel, additional, Li, Wenqing, additional, Zuurbier, Linda, additional, Silva, Milene C, additional, Paganin, Maddalena, additional, Tritapoe, Julia, additional, Hixon, Julie A, additional, Silveira, André B, additional, Cardoso, Bruno A, additional, Sarmento, Leonor M, additional, Correia, Nádia, additional, Toribio, Maria L, additional, Kobarg, Jörg, additional, Horstmann, Martin, additional, Pieters, Rob, additional, Brandalise, Silvia R, additional, Ferrando, Adolfo A, additional, Meijerink, Jules P, additional, Durum, Scott K, additional, Yunes, J Andrés, additional, and Barata, João T, additional

Published
2011
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37. Human Vδ2+ γδT cells differentially induce maturation, cytokine production, and alloreactive T cell stimulation by dendritic cells and B cells.

Author

Petrasca, Andreea, Doherty, Derek G., Dieli, Francesco, and Toribio, Maria L.

Subjects
T cells, T cell receptors, DENDRITIC cells, ANTIGEN presenting cells, B cells, CYTOKINES
Abstract

Human γδ T cells expressing the Vγ9Vδ2 T cell receptor can induce maturation of dendritic cells (DC) into antigen-presenting cells (APC) and B cells into antibody-secreting plasma cells. Since B cells are capable of presenting antigens toT cells, we investigated if Vγ9Vδ2 T cells can influence antigen-presentation by these cells. We report that Vγ9Vδ2 T cells induced expression of CD86, HLA-DR, and CD40 by B cells and stimulated the release of IL-4, IL-6,TNF-α, and IgG, IgA, and IgM. Vγ9Vδ2T cells also augmented the ability of B cells to stimulate proliferation but not IFN-γ or IL-4 release by alloreactive T cells. In contrast, Vγ9Vδ2T cells induced expression of CD86 and HLA-DR and the release of IFN-γ, IL-6, and TNF-α by DC and these DC stimulated proliferation and IFN-γ production by conventional T cells. Furthermore, CD86, TNF-α, IFN-γ, and cell contact were found to be important in DC activation by Vγ9Vδ2T cells but not in the activation of B cells. These data suggest that Vγ9Vδ2 T cells can induce maturation of B cells and DC into APC, but while they prime DC to stimulate T helper 1 (TH1) responses, they drive maturation of B cells into APC that can stimulate different T cell responses. Thus, Vγ9Vδ2 T cells can control different arms of the immune system through selective activation of B cells and DC in vitro, which may have important applications in immunotherapy and for vaccine adjuvants. [ABSTRACT FROM AUTHOR]

Published
2014
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42. Therapeutic potential of an anti-CCR9 mAb evidenced in xenografts of human CCR9 + tumors.

Author

Santamaria S, Delgado M, Botas M, Castellano E, Corraliza-Gorjon I, Lafuente P, Muñoz-Calleja C, Toribio ML, Kremer L, and Garcia-Sanz JA

Subjects
Animals, Heterografts, Humans, Mice, Receptors, CCR metabolism, Adenocarcinoma, Pancreatic Neoplasms, Precursor T-Cell Lymphoblastic Leukemia-Lymphoma
Abstract

Relapsed or refractory T acute lymphoblastic leukemia (T-ALL) still carries poor prognosis. Aiming to improve outcomes, the therapeutic potential of an anti-CCR9 monoclonal antibody (mAb 92R), targeting the human chemokine-receptor CCR9 is analyzed on orthotopic xenotransplants. 92R mAb treatment of mice carrying human CCR9 + T-ALL cell lines or primary T cell leukemias inhibits tumor growth and increases survival. The therapeutic effects of 92R are specific and synergize with chemotherapeutic agents increasing survival. Furthermore, 92R decreases size of non-hematopoietic tumors with a forced CCR9 expression and of solid tumors generated by the pancreatic adenocarcinoma cell line AsPC-1. In addition, a humanized version of 92R mAb (Srb1) is also able to inhibit growth of CCR9 + T-ALL tumor cells in vivo , increasing survival 2.66-fold. Finally, 92R mAb prevents liver accumulation of infiltrates and reduces tumor cell numbers in already formed infiltrates. Thus, the humanized version of 92R mAb (Srb1), displays therapeutic potential for CCR9 + tumor treatment and might represent one of the first therapeutic antibodies for precision medicine on T-ALL patients., Competing Interests: 92R mAb was generated by the lab of LK and developed by the labs of LK and JG-S and has been protected by the CSIC (US Patent 10,401,363; EP13382469.8); an additional patent application has been filed by the CSIC and SunRock Biopharma, Ltd. on the use of 92R in Srb1 in combination therapies for cancer (EP21382020.2). SunRock Biopharma, Ltd. (Santiago de Compostela, Spain) kindly provided the Srb1 antibody used for these experiments. Neither the financing bodies, the CSIC or SunRock Biopharma Ltd., had a role on the design of the study, data collection and analysis, nor in the decision to publish the manuscript. Therefore, the authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Santamaria, Delgado, Botas, Castellano, Corraliza-Gorjon, Lafuente, Muñoz-Calleja, Toribio, Kremer and Garcia-Sanz.)

Published
2022
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