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28 results on '"Das, Arundhoti"'

4. Transcription factor Tox2 is required for metabolic adaptation and tissue residency of ILC3 in the gut

Author

Das, Arundhoti, Martinez-Ruiz, Gustavo Ulises, Bouladoux, Nicolas, Stacy, Apollo, Moraly, Josquin, Vega-Sendino, Maria, Zhao, Yongge, Lavaert, Marieke, Ding, Yi, Morales-Sanchez, Abigail, Harly, Christelle, Seedhom, Mina O., Chari, Raj, Awasthi, Parirokh, Ikeuchi, Tomoko, Wang, Yueqiang, Zhu, Jinfang, Moutsopoulos, Niki M., Chen, WanJun, Yewdell, Jonathan W., Shapiro, Virginia Smith, Ruiz, Sergio, Taylor, Naomi, Belkaid, Yasmine, and Bhandoola, Avinash

Published
2024
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5. ILC Differentiation from Progenitors in the Bone Marrow

Author

Das, Arundhoti, Harly, Christelle, Ding, Yi, Bhandoola, Avinash, Crusio, Wim E., Series Editor, Dong, Haidong, Series Editor, Radeke, Heinfried H., Series Editor, Rezaei, Nima, Series Editor, Steinlein, Ortrud, Series Editor, Xiao, Junjie, Series Editor, and Sun, Xiao-Hong, editor

Published
2022
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7. TOX and TOX2 transcription factors cooperate with NR4A transcription factors to impose CD8+ T cell exhaustion

Author

Seo, Hyungseok, Chen, Joyce, González-Avalos, Edahí, Samaniego-Castruita, Daniela, Das, Arundhoti, Wang, Yueqiang H, López-Moyado, Isaac F, Georges, Romain O, Zhang, Wade, Onodera, Atsushi, Wu, Cheng-Jang, Lu, Li-Fan, Hogan, Patrick G, Bhandoola, Avinash, and Rao, Anjana

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Immunology, Vaccine Related, Cancer, Animals, CD8-Positive T-Lymphocytes, Immunotherapy, Lymphocyte Depletion, Lymphocytes, Tumor-Infiltrating, Mice, Mice, Inbred C57BL, Neoplasms, Protein Binding, RNA, Messenger, Transcription Factors, Tumor Microenvironment, TOX, TOX2, NR4A, NFAT, CD8(+) T cell hyporesponsiveness, CD8+ T cell hyporesponsiveness
Abstract

T cells expressing chimeric antigen receptors (CAR T cells) have shown impressive therapeutic efficacy against leukemias and lymphomas. However, they have not been as effective against solid tumors because they become hyporesponsive ("exhausted" or "dysfunctional") within the tumor microenvironment, with decreased cytokine production and increased expression of several inhibitory surface receptors. Here we define a transcriptional network that mediates CD8+ T cell exhaustion. We show that the high-mobility group (HMG)-box transcription factors TOX and TOX2, as well as members of the NR4A family of nuclear receptors, are targets of the calcium/calcineurin-regulated transcription factor NFAT, even in the absence of its partner AP-1 (FOS-JUN). Using a previously established CAR T cell model, we show that TOX and TOX2 are highly induced in CD8+ CAR+ PD-1high TIM3high ("exhausted") tumor-infiltrating lymphocytes (CAR TILs), and CAR TILs deficient in both TOX and TOX2 (Tox DKO) are more effective than wild-type (WT), TOX-deficient, or TOX2-deficient CAR TILs in suppressing tumor growth and prolonging survival of tumor-bearing mice. Like NR4A-deficient CAR TILs, Tox DKO CAR TILs show increased cytokine expression, decreased expression of inhibitory receptors, and increased accessibility of regions enriched for motifs that bind activation-associated nuclear factor κB (NFκB) and basic region-leucine zipper (bZIP) transcription factors. These data indicate that Tox and Nr4a transcription factors are critical for the transcriptional program of CD8+ T cell exhaustion downstream of NFAT. We provide evidence for positive regulation of NR4A by TOX and of TOX by NR4A, and suggest that disruption of TOX and NR4A expression or activity could be promising strategies for cancer immunotherapy.

Published
2019

10. Expression of the transcription factor Klf6 by thymic epithelial cells is required for thymus development

Author

Malin, Justin, primary, Martinez-Ruiz, Gustavo Ulises, additional, Zhao, Yongge, additional, Shissler, Susannah C., additional, Cowan, Jennifer E., additional, Ding, Yi, additional, Morales-Sanchez, Abigail, additional, Ishikawa, Masaki, additional, Lavaert, Marieke, additional, Das, Arundhoti, additional, Butcher, Donna, additional, Warner, Andrew C., additional, Kallarakal, Melissa, additional, Chen, Jingqiu, additional, Kedei, Noemi, additional, Kelly, Michael, additional, Brinster, Lauren R., additional, Allman, David, additional, and Bhandoola, Avinash, additional

Published
2023
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15. The histone demethylase Lsd1 regulates multiple repressive gene programs during T cell development

Author

Stamos, Daniel B., primary, Clubb, Lauren M., additional, Mitra, Apratim, additional, Chopp, Laura B., additional, Nie, Jia, additional, Ding, Yi, additional, Das, Arundhoti, additional, Venkataganesh, Harini, additional, Lee, Jan, additional, El-Khoury, Dalal, additional, Li, LiQi, additional, Bhandoola, Avinash, additional, Bosselut, Remy, additional, and Love, Paul E., additional

Published
2021
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19. TOX and TOX2 transcription factors cooperate with NR4A transcription factors to impose CD8 + T cell exhaustion

Author

Seo, Hyungseok, primary, Chen, Joyce, additional, González-Avalos, Edahí, additional, Samaniego-Castruita, Daniela, additional, Das, Arundhoti, additional, Wang, Yueqiang H., additional, López-Moyado, Isaac F., additional, Georges, Romain O., additional, Zhang, Wade, additional, Onodera, Atsushi, additional, Wu, Cheng-Jang, additional, Lu, Li-Fan, additional, Hogan, Patrick G., additional, Bhandoola, Avinash, additional, and Rao, Anjana, additional

Published
2019
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20. Dominant activating RAC2 mutation with lymphopenia, immunodeficiency, and cytoskeletal defects

Author

Hsu, Amy P., primary, Donkó, Agnes, additional, Arrington, Megan E., additional, Swamydas, Muthulekha, additional, Fink, Danielle, additional, Das, Arundhoti, additional, Escobedo, Omar, additional, Bonagura, Vincent, additional, Szabolcs, Paul, additional, Steinberg, Harry N., additional, Bergerson, Jenna, additional, Skoskiewicz, Amanda, additional, Makhija, Melanie, additional, Davis, Joie, additional, Foruraghi, Ladan, additional, Palmer, Cindy, additional, Fuleihan, Ramsay L., additional, Church, Joseph A., additional, Bhandoola, Avinash, additional, Lionakis, Michail S., additional, Campbell, Sharon, additional, Leto, Thomas L., additional, Kuhns, Douglas B., additional, and Holland, Steven M., additional

Published
2019
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24. TOX and TOX2 transcription factors cooperate with NR4A transcription factors to impose CD8+ T cell exhaustion.

Author

Hyungseok Seo, Chen, Joyce, González-Avalos, Edahí, Samaniego-Castruita, Daniela, Das, Arundhoti, Wang, Yueqiang H., López-Moyado, Isaac F., Georges, Romain O., Wade Zhang, Onodera, Atsushi, Cheng-Jang Wu, Li-Fan Lu, Hogan, Patrick G., Bhandoola, Avinash, and Rao, Anjana

Subjects
T cells, TRANSCRIPTION factors, NUCLEAR receptors (Biochemistry), CHIMERIC antigen receptors, GENE regulatory networks
Abstract

T cells expressing chimeric antigen receptors (CAR T cells) have shown impressive therapeutic efficacy against leukemias and lymphomas. However, they have not been as effective against solid tumors because they become hyporesponsive ("exhausted" or "dysfunctional") within the tumor microenvironment, with decreased cytokine production and increased expression of several inhibitory surface receptors. Here we define a transcriptional network that mediates CD8+ T cell exhaustion. We show that the high-mobility group (HMG)-box transcription factors TOX and TOX2, as well as members of the NR4A family of nuclear receptors, are targets of the calcium/calcineurin-regulated transcription factor NFAT, even in the absence of its partner AP-1 (FOS-JUN). Using a previously established CAR T cell model, we show that TOX and TOX2 are highly induced in CD8+ CAR+ PD-1high TIM3high ("exhausted") tumor-infiltrating lymphocytes (CAR TILs), and CAR TILs deficient in both TOX and TOX2 (Tox DKO) are more effective than wild-type (WT), TOX-deficient, or TOX2-deficient CAR TILs in suppressing tumor growth and prolonging survival of tumor-bearing mice. Like NR4A-deficient CAR TILs, Tox DKO CAR TILs show increased cytokine expression, decreased expression of inhibitory receptors, and increased accessibility of regions enriched for motifs that bind activation- associated nuclear factor êB (NFêB) and basic region-leucine zipper (bZIP) transcription factors. These data indicate that Tox and Nr4a transcription factors are critical for the transcriptional program of CD8+ T cell exhaustion downstream of NFAT. We provide evidence for positive regulation of NR4A by TOX and of TOX by NR4A, and suggest that disruption of TOX and NR4A expression or activity could be promising strategies for cancer immunotherapy. [ABSTRACT FROM AUTHOR]

Published
2019
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25. A role for MHC-mediated signalling in the functional and phenotypic heterogeneity of naive T cells (IRC8P.454)

Author

Rath, Satyajit, primary, Rane, Sanket, additional, Das, Rituparna, additional, Gund, Rupali, additional, Balyan, Renu, additional, Das, Arundhoti, additional, Khalsa, Jasneet, additional, Ranganathan, Vidya, additional, Prabhu, Savit, additional, Mattoo, Hamid, additional, Durdik, Jeannine, additional, George, Anna, additional, and Bal, Vineeta, additional

Published
2015
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27. Single-cell analysis of RORα tracer mouse lung reveals ILC progenitors and effector ILC2 subsets

Author

Ghaedi, Maryam, Shen, Zi Yi, Orangi, Mona, Martinez-Gonzalez, Itziar, Wei, Lisa, Lu, Xiaoxiao, Das, Arundhoti, Heravi-Moussavi, Alireza, Marra, Marco A., Bhandoola, Avinash, and Takei, Fumio

Abstract

Lung group 2 innate lymphoid cells (ILC2s) drive allergic inflammation and promote tissue repair. ILC2 development is dependent on the transcription factor retinoic acid receptor–related orphan receptor (RORα), which is also expressed in common ILC progenitors. To elucidate the developmental pathways of lung ILC2s, we generated RORα lineage tracer mice and performed single-cell RNA sequencing, flow cytometry, and functional analyses. In adult mouse lungs, we found an IL-18Rα+ST2− population different from conventional IL-18Rα−ST2+ ILC2s. The former was GATA-3intTcf7EGFP+Kit+, produced few cytokines, and differentiated into multiple ILC lineages in vivo and in vitro. In neonatal mouse lungs, three ILC populations were identified, namely an ILC progenitor population similar to that in adult lungs and two distinct effector ILC2 subsets that differentially produced type 2 cytokines and amphiregulin. Lung ILC progenitors might actively contribute to ILC-poiesis in neonatal and inflamed adult lungs. In addition, neonatal lung ILC2s include distinct proinflammatory and tissue-repairing subsets.

Published
2020
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28. Early Development of Innate Lymphoid Cells.

Author

Ding Y, Harly C, Das A, and Bhandoola A

Subjects
T-Lymphocytes, Immunity, Innate, Lymphocytes
Abstract

Innate lymphoid cells (ILCs) are transcriptionally and functionally similar to T cells but lack adaptive antigen receptors. They play critical roles in early defense against pathogens. In this review, we summarize recent discoveries of ILC progenitors and discuss possible mechanisms that separate ILCs from T cells. We consider mechanisms of lineage specification in early ILC development and also examine whether differences exist between adult and fetal ILC development., (© 2023. This is a U.S. government work and not under copyright protection in the U.S.; foreign copyright protection may apply.)

Published
2023
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