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121 results on '"Li, Haiyan S."'

8. Supplementary Methods, Figure Legends, Tables S1 - S3 from Loss of PTEN Promotes Resistance to T Cell–Mediated Immunotherapy

Author

Peng, Weiyi, primary, Chen, Jie Qing, primary, Liu, Chengwen, primary, Malu, Shruti, primary, Creasy, Caitlin, primary, Tetzlaff, Michael T., primary, Xu, Chunyu, primary, McKenzie, Jodi A., primary, Zhang, Chunlei, primary, Liang, Xiaoxuan, primary, Williams, Leila J., primary, Deng, Wanleng, primary, Chen, Guo, primary, Mbofung, Rina, primary, Lazar, Alexander J., primary, Torres-Cabala, Carlos A., primary, Cooper, Zachary A., primary, Chen, Pei-Ling, primary, Tieu, Trang N., primary, Spranger, Stefani, primary, Yu, Xiaoxing, primary, Bernatchez, Chantale, primary, Forget, Marie-Andree, primary, Haymaker, Cara, primary, Amaria, Rodabe, primary, McQuade, Jennifer L., primary, Glitza, Isabella C., primary, Cascone, Tina, primary, Li, Haiyan S., primary, Kwong, Lawrence N., primary, Heffernan, Timothy P., primary, Hu, Jianhua, primary, Bassett, Roland L., primary, Bosenberg, Marcus W., primary, Woodman, Scott E., primary, Overwijk, Willem W., primary, Lizée, Gregory, primary, Roszik, Jason, primary, Gajewski, Thomas F., primary, Wargo, Jennifer A., primary, Gershenwald, Jeffrey E., primary, Radvanyi, Laszlo, primary, Davies, Michael A., primary, and Hwu, Patrick, primary

Published
2023
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9. Supplementary Figure S7 from Loss of PTEN Promotes Resistance to T Cell–Mediated Immunotherapy

Author

Peng, Weiyi, primary, Chen, Jie Qing, primary, Liu, Chengwen, primary, Malu, Shruti, primary, Creasy, Caitlin, primary, Tetzlaff, Michael T., primary, Xu, Chunyu, primary, McKenzie, Jodi A., primary, Zhang, Chunlei, primary, Liang, Xiaoxuan, primary, Williams, Leila J., primary, Deng, Wanleng, primary, Chen, Guo, primary, Mbofung, Rina, primary, Lazar, Alexander J., primary, Torres-Cabala, Carlos A., primary, Cooper, Zachary A., primary, Chen, Pei-Ling, primary, Tieu, Trang N., primary, Spranger, Stefani, primary, Yu, Xiaoxing, primary, Bernatchez, Chantale, primary, Forget, Marie-Andree, primary, Haymaker, Cara, primary, Amaria, Rodabe, primary, McQuade, Jennifer L., primary, Glitza, Isabella C., primary, Cascone, Tina, primary, Li, Haiyan S., primary, Kwong, Lawrence N., primary, Heffernan, Timothy P., primary, Hu, Jianhua, primary, Bassett, Roland L., primary, Bosenberg, Marcus W., primary, Woodman, Scott E., primary, Overwijk, Willem W., primary, Lizée, Gregory, primary, Roszik, Jason, primary, Gajewski, Thomas F., primary, Wargo, Jennifer A., primary, Gershenwald, Jeffrey E., primary, Radvanyi, Laszlo, primary, Davies, Michael A., primary, and Hwu, Patrick, primary

Published
2023
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10. Data from Loss of PTEN Promotes Resistance to T Cell–Mediated Immunotherapy

Author

Peng, Weiyi, primary, Chen, Jie Qing, primary, Liu, Chengwen, primary, Malu, Shruti, primary, Creasy, Caitlin, primary, Tetzlaff, Michael T., primary, Xu, Chunyu, primary, McKenzie, Jodi A., primary, Zhang, Chunlei, primary, Liang, Xiaoxuan, primary, Williams, Leila J., primary, Deng, Wanleng, primary, Chen, Guo, primary, Mbofung, Rina, primary, Lazar, Alexander J., primary, Torres-Cabala, Carlos A., primary, Cooper, Zachary A., primary, Chen, Pei-Ling, primary, Tieu, Trang N., primary, Spranger, Stefani, primary, Yu, Xiaoxing, primary, Bernatchez, Chantale, primary, Forget, Marie-Andree, primary, Haymaker, Cara, primary, Amaria, Rodabe, primary, McQuade, Jennifer L., primary, Glitza, Isabella C., primary, Cascone, Tina, primary, Li, Haiyan S., primary, Kwong, Lawrence N., primary, Heffernan, Timothy P., primary, Hu, Jianhua, primary, Bassett, Roland L., primary, Bosenberg, Marcus W., primary, Woodman, Scott E., primary, Overwijk, Willem W., primary, Lizée, Gregory, primary, Roszik, Jason, primary, Gajewski, Thomas F., primary, Wargo, Jennifer A., primary, Gershenwald, Jeffrey E., primary, Radvanyi, Laszlo, primary, Davies, Michael A., primary, and Hwu, Patrick, primary

Published
2023
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11. Supplementary Figure 3 from BRAF Inhibition Increases Tumor Infiltration by T cells and Enhances the Antitumor Activity of Adoptive Immunotherapy in Mice

Author

Liu, Chengwen, primary, Peng, Weiyi, primary, Xu, Chunyu, primary, Lou, Yanyan, primary, Zhang, Minying, primary, Wargo, Jennifer A., primary, Chen, Jie Qing, primary, Li, Haiyan S., primary, Watowich, Stephanie S., primary, Yang, Yan, primary, Frederick, Dennie Tompers, primary, Cooper, Zachary A., primary, Mbofung, Rina M., primary, Whittington, Mayra, primary, Flaherty, Keith T., primary, Woodman, Scott E., primary, Davies, Michael A., primary, Radvanyi, Laszlo G., primary, Overwijk, Willem W., primary, Lizée, Gregory, primary, and Hwu, Patrick, primary

Published
2023
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12. Supplementary Figure 1 from BRAF Inhibition Increases Tumor Infiltration by T cells and Enhances the Antitumor Activity of Adoptive Immunotherapy in Mice

Author

Liu, Chengwen, primary, Peng, Weiyi, primary, Xu, Chunyu, primary, Lou, Yanyan, primary, Zhang, Minying, primary, Wargo, Jennifer A., primary, Chen, Jie Qing, primary, Li, Haiyan S., primary, Watowich, Stephanie S., primary, Yang, Yan, primary, Frederick, Dennie Tompers, primary, Cooper, Zachary A., primary, Mbofung, Rina M., primary, Whittington, Mayra, primary, Flaherty, Keith T., primary, Woodman, Scott E., primary, Davies, Michael A., primary, Radvanyi, Laszlo G., primary, Overwijk, Willem W., primary, Lizée, Gregory, primary, and Hwu, Patrick, primary

Published
2023
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13. Supplementary Figure 9 from BRAF Inhibition Increases Tumor Infiltration by T cells and Enhances the Antitumor Activity of Adoptive Immunotherapy in Mice

Author

Liu, Chengwen, primary, Peng, Weiyi, primary, Xu, Chunyu, primary, Lou, Yanyan, primary, Zhang, Minying, primary, Wargo, Jennifer A., primary, Chen, Jie Qing, primary, Li, Haiyan S., primary, Watowich, Stephanie S., primary, Yang, Yan, primary, Frederick, Dennie Tompers, primary, Cooper, Zachary A., primary, Mbofung, Rina M., primary, Whittington, Mayra, primary, Flaherty, Keith T., primary, Woodman, Scott E., primary, Davies, Michael A., primary, Radvanyi, Laszlo G., primary, Overwijk, Willem W., primary, Lizée, Gregory, primary, and Hwu, Patrick, primary

Published
2023
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14. Supplementary Figure 7 from BRAF Inhibition Increases Tumor Infiltration by T cells and Enhances the Antitumor Activity of Adoptive Immunotherapy in Mice

Author

Liu, Chengwen, primary, Peng, Weiyi, primary, Xu, Chunyu, primary, Lou, Yanyan, primary, Zhang, Minying, primary, Wargo, Jennifer A., primary, Chen, Jie Qing, primary, Li, Haiyan S., primary, Watowich, Stephanie S., primary, Yang, Yan, primary, Frederick, Dennie Tompers, primary, Cooper, Zachary A., primary, Mbofung, Rina M., primary, Whittington, Mayra, primary, Flaherty, Keith T., primary, Woodman, Scott E., primary, Davies, Michael A., primary, Radvanyi, Laszlo G., primary, Overwijk, Willem W., primary, Lizée, Gregory, primary, and Hwu, Patrick, primary

Published
2023
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15. Supplementary Figure Legend from BRAF Inhibition Increases Tumor Infiltration by T cells and Enhances the Antitumor Activity of Adoptive Immunotherapy in Mice

Author

Liu, Chengwen, primary, Peng, Weiyi, primary, Xu, Chunyu, primary, Lou, Yanyan, primary, Zhang, Minying, primary, Wargo, Jennifer A., primary, Chen, Jie Qing, primary, Li, Haiyan S., primary, Watowich, Stephanie S., primary, Yang, Yan, primary, Frederick, Dennie Tompers, primary, Cooper, Zachary A., primary, Mbofung, Rina M., primary, Whittington, Mayra, primary, Flaherty, Keith T., primary, Woodman, Scott E., primary, Davies, Michael A., primary, Radvanyi, Laszlo G., primary, Overwijk, Willem W., primary, Lizée, Gregory, primary, and Hwu, Patrick, primary

Published
2023
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16. Supplementary Figure 5 from BRAF Inhibition Increases Tumor Infiltration by T cells and Enhances the Antitumor Activity of Adoptive Immunotherapy in Mice

Author

Liu, Chengwen, primary, Peng, Weiyi, primary, Xu, Chunyu, primary, Lou, Yanyan, primary, Zhang, Minying, primary, Wargo, Jennifer A., primary, Chen, Jie Qing, primary, Li, Haiyan S., primary, Watowich, Stephanie S., primary, Yang, Yan, primary, Frederick, Dennie Tompers, primary, Cooper, Zachary A., primary, Mbofung, Rina M., primary, Whittington, Mayra, primary, Flaherty, Keith T., primary, Woodman, Scott E., primary, Davies, Michael A., primary, Radvanyi, Laszlo G., primary, Overwijk, Willem W., primary, Lizée, Gregory, primary, and Hwu, Patrick, primary

Published
2023
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17. Supplementary Figure 2 from BRAF Inhibition Increases Tumor Infiltration by T cells and Enhances the Antitumor Activity of Adoptive Immunotherapy in Mice

Author

Liu, Chengwen, primary, Peng, Weiyi, primary, Xu, Chunyu, primary, Lou, Yanyan, primary, Zhang, Minying, primary, Wargo, Jennifer A., primary, Chen, Jie Qing, primary, Li, Haiyan S., primary, Watowich, Stephanie S., primary, Yang, Yan, primary, Frederick, Dennie Tompers, primary, Cooper, Zachary A., primary, Mbofung, Rina M., primary, Whittington, Mayra, primary, Flaherty, Keith T., primary, Woodman, Scott E., primary, Davies, Michael A., primary, Radvanyi, Laszlo G., primary, Overwijk, Willem W., primary, Lizée, Gregory, primary, and Hwu, Patrick, primary

Published
2023
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18. Supplementary Figure 4 from BRAF Inhibition Increases Tumor Infiltration by T cells and Enhances the Antitumor Activity of Adoptive Immunotherapy in Mice

Author

Liu, Chengwen, primary, Peng, Weiyi, primary, Xu, Chunyu, primary, Lou, Yanyan, primary, Zhang, Minying, primary, Wargo, Jennifer A., primary, Chen, Jie Qing, primary, Li, Haiyan S., primary, Watowich, Stephanie S., primary, Yang, Yan, primary, Frederick, Dennie Tompers, primary, Cooper, Zachary A., primary, Mbofung, Rina M., primary, Whittington, Mayra, primary, Flaherty, Keith T., primary, Woodman, Scott E., primary, Davies, Michael A., primary, Radvanyi, Laszlo G., primary, Overwijk, Willem W., primary, Lizée, Gregory, primary, and Hwu, Patrick, primary

Published
2023
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19. Supplementary Figure 8 from BRAF Inhibition Increases Tumor Infiltration by T cells and Enhances the Antitumor Activity of Adoptive Immunotherapy in Mice

Author

Liu, Chengwen, primary, Peng, Weiyi, primary, Xu, Chunyu, primary, Lou, Yanyan, primary, Zhang, Minying, primary, Wargo, Jennifer A., primary, Chen, Jie Qing, primary, Li, Haiyan S., primary, Watowich, Stephanie S., primary, Yang, Yan, primary, Frederick, Dennie Tompers, primary, Cooper, Zachary A., primary, Mbofung, Rina M., primary, Whittington, Mayra, primary, Flaherty, Keith T., primary, Woodman, Scott E., primary, Davies, Michael A., primary, Radvanyi, Laszlo G., primary, Overwijk, Willem W., primary, Lizée, Gregory, primary, and Hwu, Patrick, primary

Published
2023
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20. Supplementary Figure 6 from BRAF Inhibition Increases Tumor Infiltration by T cells and Enhances the Antitumor Activity of Adoptive Immunotherapy in Mice

Author

Liu, Chengwen, primary, Peng, Weiyi, primary, Xu, Chunyu, primary, Lou, Yanyan, primary, Zhang, Minying, primary, Wargo, Jennifer A., primary, Chen, Jie Qing, primary, Li, Haiyan S., primary, Watowich, Stephanie S., primary, Yang, Yan, primary, Frederick, Dennie Tompers, primary, Cooper, Zachary A., primary, Mbofung, Rina M., primary, Whittington, Mayra, primary, Flaherty, Keith T., primary, Woodman, Scott E., primary, Davies, Michael A., primary, Radvanyi, Laszlo G., primary, Overwijk, Willem W., primary, Lizée, Gregory, primary, and Hwu, Patrick, primary

Published
2023
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22. Intestinal toxicity to CTLA-4 blockade driven by IL-6 and myeloid infiltration

Author

Zhou, Yifan, primary, Medik, Yusra B., additional, Patel, Bhakti, additional, Zamler, Daniel B., additional, Chen, Sijie, additional, Chapman, Thomas, additional, Schneider, Sarah, additional, Park, Elizabeth M., additional, Babcock, Rachel L., additional, Chrisikos, Taylor T., additional, Kahn, Laura M., additional, Dyevoich, Allison M., additional, Pineda, Josue E., additional, Wong, Matthew C., additional, Mishra, Aditya K., additional, Cass, Samuel H., additional, Cogdill, Alexandria P., additional, Johnson, Daniel H., additional, Johnson, Sarah B., additional, Wani, Khalida, additional, Ledesma, Debora A., additional, Hudgens, Courtney W., additional, Wang, Jingjing, additional, Wadud Khan, Md Abdul, additional, Peterson, Christine B., additional, Joon, Aron Y., additional, Peng, Weiyi, additional, Li, Haiyan S., additional, Arora, Reetakshi, additional, Tang, Ximing, additional, Raso, Maria Gabriela, additional, Zhang, Xuegong, additional, Foo, Wai Chin, additional, Tetzlaff, Michael T., additional, Diehl, Gretchen E., additional, Clise-Dwyer, Karen, additional, Whitley, Elizabeth M., additional, Gubin, Matthew M., additional, Allison, James P., additional, Hwu, Patrick, additional, Ajami, Nadim J., additional, Diab, Adi, additional, Wargo, Jennifer A., additional, and Watowich, Stephanie S., additional

Published
2022
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23. Abstract 5545: Intestinal toxicity to CTLA-4 blockade driven by IL-6 and myeloid infiltration

Author

Zhou, Yifan, primary, Medik, Yusra B., additional, Patel, Bhakti, additional, Zamler, Daniel B., additional, Chen, Sijie, additional, Chapman, Thomas, additional, Schneider, Sarah, additional, Babcock, Rachel L., additional, Chrisikos, Taylor T., additional, Kahn, Laura M., additional, Dyevoich, Allison M., additional, Park, Elizabeth M., additional, Cogdill, Alexandria P., additional, Johnson, Daniel H., additional, Johnson, Sarah B., additional, Wani, Khalida M., additional, Ledesma, Debora A., additional, Hudgens, Courtney W., additional, Wang, Jingjing, additional, Khan, Md Abdul Wadud, additional, Joon, Aron Y., additional, Peng, Weiyi, additional, Li, Haiyan S., additional, Arora, Reetakshi, additional, Tang, Ximing, additional, Raso, Maria Gabriela, additional, Zhang, Xuegong, additional, Foo, Wai Chin, additional, Tetzlaff, Michael T., additional, Diehl, Gretchen E., additional, Clise-Dwyer, Karen, additional, Whitley, Elizabeth M., additional, Gubin, Matthew M., additional, Allison, James P., additional, Hwu, Patrick, additional, Ajami, Nadim J., additional, Diab, Adi, additional, Wargo, Jennifer A., additional, and Watowich, Stephanie S., additional

Published
2022
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25. Tonic interferon restricts pathogenic IL-17-driven inflammatory disease via balancing the microbiome

Author

Marié, Isabelle J, primary, Brambilla, Lara, additional, Azzouz, Doua, additional, Chen, Ze, additional, Baracho, Gisele V, additional, Arnett, Azlann, additional, Li, Haiyan S, additional, Liu, Weiguo, additional, Cimmino, Luisa, additional, Chattopadhyay, Pratip, additional, Silverman, Gregg, additional, Watowich, Stephanie S, additional, Khor, Bernard, additional, and Levy, David E, additional

Published
2021
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26. Author response: Tonic interferon restricts pathogenic IL-17-driven inflammatory disease via balancing the microbiome

Author

Marié, Isabelle J, primary, Brambilla, Lara, additional, Azzouz, Doua, additional, Chen, Ze, additional, Baracho, Gisele V, additional, Arnett, Azlann, additional, Li, Haiyan S, additional, Liu, Weiguo, additional, Cimmino, Luisa, additional, Chattopadhyay, Pratip, additional, Silverman, Gregg, additional, Watowich, Stephanie S, additional, Khor, Bernard, additional, and Levy, David E, additional

Published
2021
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28. Tonic interferon restricts pathogenic IL-17-driven inflammatory disease via balancing the microbiome

Author

Marié, Isabelle J., primary, Brambilla, Lara, additional, Azzouz, Doua, additional, Chen, Ze, additional, Baracho, Gisele, additional, Arnett, Azlann, additional, Li, Haiyan S., additional, Liu, Weiguo, additional, Cimmino, Luisa, additional, Chattopadhyay, Pratip, additional, Silverman, Gregg, additional, Watowich, Stephanie S., additional, Khor, Bernard, additional, and Levy, David E., additional

Published
2021
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36. PPARD and Interferon Gamma Promote Transformation of Gastric Progenitor Cells and Tumorigenesis in Mice

Author

Zuo, Xiangsheng, primary, Deguchi, Yasunori, additional, Xu, Weiguo, additional, Liu, Yi, additional, Li, Haiyan S., additional, Wei, Daoyan, additional, Tian, Rui, additional, Chen, Weidong, additional, Xu, Min, additional, Yang, Yaying, additional, Gao, Shen, additional, Jaoude, Jonathan C., additional, Liu, Fuyao, additional, Chrieki, Sarah P., additional, Moussalli, Micheline J., additional, Gagea, Mihai, additional, Sebastian, Manu M., additional, Zheng, Xiaofeng, additional, Tan, Dongfeng, additional, Broaddus, Russell, additional, Wang, Jing, additional, Ajami, Nadim J., additional, Swennes, Alton G., additional, Watowich, Stephanie S., additional, and Shureiqi, Imad, additional

Published
2019
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37. The kinase TBK1 functions in dendritic cells to regulate T cell homeostasis, autoimmunity, and antitumor immunity

Author

Xiao, Yichuan, primary, Zou, Qiang, additional, Xie, Xiaoping, additional, Liu, Ting, additional, Li, Haiyan S., additional, Jie, Zuliang, additional, Jin, Jin, additional, Hu, Hongbo, additional, Manyam, Ganiraju, additional, Zhang, Li, additional, Cheng, Xuhong, additional, Wang, Hui, additional, Marie, Isabelle, additional, Levy, David E., additional, Watowich, Stephanie S., additional, and Sun, Shao-Cong, additional

Published
2017
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40. Loss of PTEN Promotes Resistance to T Cell–Mediated Immunotherapy

Author

Peng, Weiyi, primary, Chen, Jie Qing, additional, Liu, Chengwen, additional, Malu, Shruti, additional, Creasy, Caitlin, additional, Tetzlaff, Michael T., additional, Xu, Chunyu, additional, McKenzie, Jodi A., additional, Zhang, Chunlei, additional, Liang, Xiaoxuan, additional, Williams, Leila J., additional, Deng, Wanleng, additional, Chen, Guo, additional, Mbofung, Rina, additional, Lazar, Alexander J., additional, Torres-Cabala, Carlos A., additional, Cooper, Zachary A., additional, Chen, Pei-Ling, additional, Tieu, Trang N., additional, Spranger, Stefani, additional, Yu, Xiaoxing, additional, Bernatchez, Chantale, additional, Forget, Marie-Andree, additional, Haymaker, Cara, additional, Amaria, Rodabe, additional, McQuade, Jennifer L., additional, Glitza, Isabella C., additional, Cascone, Tina, additional, Li, Haiyan S., additional, Kwong, Lawrence N., additional, Heffernan, Timothy P., additional, Hu, Jianhua, additional, Bassett, Roland L., additional, Bosenberg, Marcus W., additional, Woodman, Scott E., additional, Overwijk, Willem W., additional, Lizée, Gregory, additional, Roszik, Jason, additional, Gajewski, Thomas F., additional, Wargo, Jennifer A., additional, Gershenwald, Jeffrey E., additional, Radvanyi, Laszlo, additional, Davies, Michael A., additional, and Hwu, Patrick, additional

Published
2016
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42. Genetic rescue of lineage-balanced blood cell production reveals a crucial role for STAT3 antiinflammatory activity in hematopoiesis.

Author

Huiyuan Zhang, Li, Haiyan S., Hillmer, Emily J., Yang Zhao, Chrisikos, Taylor T., Hongbo Hu, Xiao Wu, Thompson, Erika J., Clise-Dwyer, Karen, Millerchip, Karen A., Yue Wei, Puebla-Osorio, Nahum, Kaushik, Saakshi, Santos, Margarida A., Bin Wang, Garcia-Manero, Guillermo, Jing Wang, Shao-Cong Sun, and Watowich, Stephanie S.

Subjects
*HEMATOPOIESIS, *BLOOD cells, *HEMOSTASIS, *STAT proteins, *ANTI-inflammatory agents
Abstract

Blood cell formation must be appropriately maintained throughout life to provide robust immune function, hemostasis, and oxygen delivery to tissues, and to prevent disorders that result from over- or underproduction of critical lineages. Persistent inflammation deregulates hematopoiesis by damaging hematopoietic stem and progenitor cells (HSPCs), leading to elevated myeloid cell output and eventual bone marrow failure. Nonetheless, antiinflammatory mechanisms that protect the hematopoietic system are understudied. The transcriptional regulator STAT3 has myriad roles in HSPC-derived populations and nonhematopoietic tissues, including a potent antiinflammatory function in differentiated myeloid cells. STAT3 antiinflammatory activity is facilitated by STAT3-mediated transcriptional repression of Ube2n, which encodes the E2 ubiquitin-conjugating enzyme Ubc13 involved in proinflammatory signaling. Here we demonstrate a crucial role for STAT3 antiinflammatory activity in preservation of HSPCs and lineage-balanced hematopoiesis. Conditional Stat3 removal from the hematopoietic system led to depletion of the bone marrow lineage- Sca-1+ c-Kit+ CD150+ CD48- HSPC subset (LSK CD150+CD48- cells), myeloid-skewed hematopoiesis, and accrual of DNA damage in HSPCs. These responses were accompanied by intrinsic transcriptional alterations in HSPCs, including deregulation of inflammatory, survival and developmental pathways. Concomitant Ube2n/Ubc13 deletion from Stat3-deficient hematopoietic cells enabled lineage-balanced hematopoiesis, mitigated depletion of bone marrow LSK CD150+ CD48- cells, alleviated HSPC DNA damage, and corrected a majority of aberrant transcriptional responses. These results indicate an intrinsic protective role for STAT3 in the hematopoietic system, and suggest that this is mediated by STAT3-dependent restraint of excessive proinflammatory signaling via Ubc13 modulation. [ABSTRACT FROM AUTHOR]

Published
2018
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43. CXCR5+CD8+T cells are a distinct functional subset with an antitumor activity

Author

Chu, Fuliang, Li, Haiyan S., Liu, Xindong, Cao, Jingjing, Ma, Wencai, Ma, Ying, Weng, Jinsheng, Zhu, Zheng, Cheng, Xiaoyun, Wang, Zhiqiang, Liu, Jingwei, Jiang, Zi Yang, Luong, Amber U., Peng, Weiyi, Wang, Jing, Balakrishnan, Kumudha, Yee, Cassian, Dong, Chen, Davis, Richard Eric, Watowich, Stephanie S., and Neelapu, Sattva S.

Abstract

CXCR5 mediates homing of both B and follicular helper T (TFH) cells into follicles of secondary lymphoid organs. We found that CXCR5+CD8+T cells are present in human tonsils and follicular lymphoma, inhibit TFH-mediated B cell differentiation, and exhibit strong cytotoxic activity. Consistent with these findings, adoptive transfer of CXCR5+CD8+T cells into an animal model of lymphoma resulted in significantly greater antitumor activity than CXCR5−CD8+T cells. Furthermore, RNA-Seq-based transcriptional profiling revealed 77 differentially expressed genes unique to CXCR5+CD8+T cells. Among these, a signature comprised of 33 upregulated genes correlated with improved survival in follicular lymphoma patients. We also showed that CXCR5+CD8+T cells could be induced and expanded ex vivo using IL-23 plus TGF-β, suggesting a possible strategy to generate these cells for clinical application. In summary, our study identified CXCR5+CD8+T cells as a distinct T cell subset with ability to suppress TFH-mediated B cell differentiation, exert strong antitumor activity, and confer favorable prognosis in follicular lymphoma patients.

Published
2019
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46. STAT3 restrains RANK- and TLR4-mediated signalling by suppressing expression of the E2 ubiquitin-conjugating enzyme Ubc13

Author

Zhang, Huiyuan, primary, Hu, Hongbo, additional, Greeley, Nathaniel, additional, Jin, Jin, additional, Matthews, Allison J, additional, Ohashi, Erika, additional, Caetano, Mauricio S., additional, Li, Haiyan S., additional, Wu, Xuefeng, additional, Mandal, Pijus K., additional, McMurray, John S., additional, Moghaddam, Seyed Javad, additional, Sun, Shao-Cong, additional, and Watowich, Stephanie S., additional

Published
2014
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47. 15-Lipoxygenase-1 suppression of colitis-associated colon cancer through inhibition of the IL-6/STAT3 signaling pathway.

Author

Fei Mao, Min Xu, Xiangsheng Zuo, Jiang Yu, Weiguo Xu, Moussalli, Micheline J., Elias, Elias, Li, Haiyan S., Watowich, Stephanie S., and Shureiqi, Imad

Subjects
INTERLEUKIN-6, TRANSCRIPTION factors, GENETICS of colon cancer, EPITHELIAL cells, PHOSPHORYLATION, GENE expression
Abstract

The IL-6/signal transducer and activator of transcription 3 (STAT3) pathway is a critical signaling pathway for colitis-associated colorectal cancer (CAC). Peroxisome proliferator-activated receptor (PPAR)-δ, a lipid nuclear receptor, up-regulates IL-6. 15-Lipoxygenase-1 (15-LOX-1), which is crucial to production of lipid signaling mediators to terminate inflammation, down-regulates PPAR-δ. 15-LOX-1 effects on IL-6/STAT3 signaling and CAC tumorigenesis have not been determined. We report that intestinally targeted transgenic 15-LOX-1 expression in mice inhibited azoxymethane- and dextran sodium sulfate--induced CAC, IL-6 expression, STAT3 phosphorylation, and IL-6/STAT3 downstream target (Notch3 and MUC1) expression. 15-LOX-1 down-regulation was associated with IL-6 up-regulation in human colon cancer mucosa. Reexpression of 15-LOX-1 in human colon cancer cells suppressed IL-6 mRNA expression, STAT3 phosphorylation, IL-6 promoter activity, and PPAR-δ mRNA and protein expression. PPAR-δ overexpression in colonic epithelial cells promoted CAC tumorigenesis in mice and increased IL-6 expression and STAT3 phosphorylation, whereas concomitant 15-LOX-1 expression in colonic epithelial cells (15-LOX-1-PPAR-δ-Gut mice) suppressed these effects: the number of tumors per mouse (mean ± SEM) was 4.22 ± 0.68 in wild-type littermates, 6.67 ± 0.83 in PPAR-δ-Gut mice (P = 0.026), and 2.25 ± 0.25 in 15-LOX-1-PPAR-δ-Gut mice (P = 0.0006). Identification of 15-LOX-1 suppression of PPAR-δ to inhibit IL-6/STAT3 signaling-driven CAC tumorigenesis provides mechanistic insights that can be used to molecularly target CAC. [ABSTRACT FROM AUTHOR]

Published
2015
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48. Intestinal toxicity to CTLA-4 blockade driven by IL-6 and myeloid infiltration

Author

Zhou, Yifan, Medik, Yusra B., Patel, Bhakti, Zamler, Daniel B., Chen, Sijie, Chapman, Thomas, Schneider, Sarah, Park, Elizabeth M., Babcock, Rachel L., Chrisikos, Taylor T., Kahn, Laura M., Dyevoich, Allison M., Pineda, Josue E., Wong, Matthew C., Mishra, Aditya K., Cass, Samuel H., Cogdill, Alexandria P., Johnson, Daniel H., Johnson, Sarah B., Wani, Khalida, Ledesma, Debora A., Hudgens, Courtney W., Wang, Jingjing, Wadud Khan, Md Abdul, Peterson, Christine B., Joon, Aron Y., Peng, Weiyi, Li, Haiyan S., Arora, Reetakshi, Tang, Ximing, Raso, Maria Gabriela, Zhang, Xuegong, Foo, Wai Chin, Tetzlaff, Michael T., Diehl, Gretchen E., Clise-Dwyer, Karen, Whitley, Elizabeth M., Gubin, Matthew M., Allison, James P., Hwu, Patrick, Ajami, Nadim J., Diab, Adi, Wargo, Jennifer A., and Watowich, Stephanie S.

Abstract

Immune checkpoint blockade (ICB) has revolutionized cancer treatment, yet quality of life and continuation of therapy can be constrained by immune-related adverse events (irAEs). Limited understanding of irAE mechanisms hampers development of approaches to mitigate their damage. To address this, we examined whether mice gained sensitivity to anti-CTLA-4 (αCTLA-4)–mediated toxicity upon disruption of gut homeostatic immunity. We found αCTLA-4 drove increased inflammation and colonic tissue damage in mice with genetic predisposition to intestinal inflammation, acute gastrointestinal infection, transplantation with a dysbiotic fecal microbiome, or dextran sodium sulfate administration. We identified an immune signature of αCTLA-4–mediated irAEs, including colonic neutrophil accumulation and systemic interleukin-6 (IL-6) release. IL-6 blockade combined with antibiotic treatment reduced intestinal damage and improved αCTLA-4 therapeutic efficacy in inflammation-prone mice. Intestinal immune signatures were validated in biopsies from patients with ICB colitis. Our work provides new preclinical models of αCTLA-4 intestinal irAEs, mechanistic insights into irAE development, and potential approaches to enhance ICB efficacy while mitigating irAEs.

Published
2023
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49. Histone Deacetylase Inhibitors and IL21 Cooperate to Reprogram Human Effector CD8 + T Cells to Memory T Cells.

Author

Wang J, Hasan F, Frey AC, Li HS, Park J, Pan K, Haymaker C, Bernatchez C, Lee DA, Watowich SS, and Yee C

Subjects
Adolescent, CD28 Antigens genetics, CD8-Positive T-Lymphocytes drug effects, CD8-Positive T-Lymphocytes metabolism, Cell Proliferation, Cells, Cultured, Humans, Immunologic Memory drug effects, Immunotherapy, Adoptive, T-Lymphocytes drug effects, T-Lymphocytes metabolism, CD28 Antigens metabolism, CD8-Positive T-Lymphocytes immunology, Cell Differentiation, Histone Deacetylase Inhibitors pharmacology, Immunologic Memory immunology, Interleukins metabolism, T-Lymphocytes immunology
Abstract

Clinical response rates after adoptive cell therapy (ACT) are highly correlated with in vivo persistence of the infused T cells. However, antigen-specific T cells found in tumor sites are often well-differentiated effector cells with limited persistence. Central memory CD8 + T cells, capable of self-renewal, represent desirable ACT products. We report here that exposure to a histone deacetylase inhibitor (HDACi) and IL21 could reprogram differentiated human CD8 + T cells into central memory-like T cells. Dedifferentiation of CD8 + T cells was initiated by increased H3 acetylation and chromatin accessibility at the CD28 promoter region. This led to IL21-mediated pSTAT3 binding to the CD28 region, and subsequent upregulation of surface CD28 and CD62L (markers of central memory T cells). The reprogrammed cells exhibited enhanced proliferation in response to both IL2 and IL15, and a stable memory-associated transcriptional signature (increased Lef1 and Tcf7 ). Our findings support the application of IL21 and HDACi for the in vitro generation of highly persistent T-cell populations that can augment the efficacy of adoptively transferred T cells., (©2020 American Association for Cancer Research.)

Published
2020
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50. Vaccine efficacy against primary and metastatic cancer with in vitro-generated CD103 + conventional dendritic cells.

Author

Zhou Y, Slone N, Chrisikos TT, Kyrysyuk O, Babcock RL, Medik YB, Li HS, Kleinerman ES, and Watowich SS

Subjects
Animals, Antigen Presentation immunology, Antigens, CD metabolism, Antigens, Neoplasm immunology, Bone Neoplasms immunology, Bone Neoplasms pathology, Bone Neoplasms therapy, Cross-Priming, Dendritic Cells transplantation, Immunotherapy, In Vitro Techniques, Integrin alpha Chains metabolism, Lung Neoplasms secondary, Lung Neoplasms therapy, Melanoma, Experimental pathology, Melanoma, Experimental therapy, Mice, Mice, Inbred C57BL, Osteosarcoma pathology, Osteosarcoma therapy, Sarcoma, Experimental pathology, Sarcoma, Experimental therapy, Tumor Cells, Cultured, Antigens, CD immunology, Dendritic Cells immunology, Integrin alpha Chains immunology, Lung Neoplasms immunology, Melanoma, Experimental immunology, Osteosarcoma immunology, Sarcoma, Experimental immunology, Vaccines administration & dosage
Abstract

Background: Type 1 conventional dendritic cells (cDC1s) possess efficient antigen presentation and cross-presentation activity, as well as potent T cell priming ability. Tissue-resident cDC1s (CD103 + cDC1s in mice, CD141 + cDC1s in humans) are linked with improved tumor control, yet the efficacy of immunotherapy using this population is understudied., Methods: We generated murine CD103 + cDC1s in vitro and examined their expression of cDC1-related factors, antigen cross-presentation activity, and accumulation in tumor-draining lymph nodes (TdLNs). The antitumor efficacy of the in vitro-generated CD103 + cDC1s was studied in murine melanoma and osteosarcoma models. We evaluated tumor responses on vaccination with CD103 + cDC1s, compared these to vaccination with monocyte-derived DCs (MoDCs), tested CD103 + cDC1 vaccination with checkpoint blockade, and examined the antimetastatic activity of CD103 + cDC1s., Results: In vitro-generated CD103 + cDC1s produced cDC1-associated factors such as interleukin-12p70 and CXCL10, and demonstrated antigen cross-presentation activity on stimulation with the toll-like receptor 3 agonist polyinosinic:polycytidylic acid (poly I:C). In vitro-generated CD103 + cDC1s also migrated to TdLNs following poly I:C treatment and intratumoral delivery. Vaccination with poly I:C-activated and tumor antigen-loaded CD103 + cDC1s enhanced tumor infiltration of tumor antigen-specific and interferon-γ + CD8 + T cells, and suppressed melanoma and osteosarcoma growth. CD103 + cDC1s showed superior antitumor efficacy compared with MoDC vaccination, and led to complete regression of 100% of osteosarcoma tumors in combination with CTLA-4 antibody-mediated checkpoint blockade. In vitro-generated CD103 + cDC1s effectively protected mice from pulmonary melanoma and osteosarcoma metastases., Conclusions: Our data indicate an in vitro-generated CD103 + cDC1 vaccine elicits systemic and long-lasting tumor-specific T cell-mediated cytotoxicity, which restrains primary and metastatic tumor growth. The CD103 + cDC1 vaccine was superior to MoDCs and enhanced response to immune checkpoint blockade. These results indicate the potential for new immunotherapies based on use of cDC1s alone or in combination with checkpoint blockade., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2020. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.)

Published
2020
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