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466 results on '"Mehrotra, Shikhar"'

12. CD38–RyR2 axis–mediated signaling impedes CD8 + T cell response to anti-PD1 therapy in cancer

Author

Kar, Anwesha, primary, Ghosh, Puspendu, additional, Gautam, Anupam, additional, Chowdhury, Snehanshu, additional, Basak, Debashree, additional, Sarkar, Ishita, additional, Bhoumik, Arpita, additional, Barman, Shubhrajit, additional, Chakraborty, Paramita, additional, Mukhopadhyay, Asima, additional, Mehrotra, Shikhar, additional, Ganesan, Senthil Kumar, additional, Paul, Sandip, additional, and Chatterjee, Shilpak, additional

Published
2024
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13. Comparative analysis of antibodies to SARS-CoV-2 between asymptomatic and convalescent patients

Author

Dwyer, Connor J., Cloud, Colleen A., Wang, Cindy, Heidt, Philip, Chakraborty, Paramita, Duke, Tara F., McGue, Shannon, Jeffcoat, Braxton, Dunne, Jaclyn, Johnson, Logan, Choi, Seungho, Nahhas, Georges J., Gandy, Amy S., Babic, Nikolina, Nolte, Frederick S., Howe, Philip, Ogretmen, Besim, Gangaraju, Vamsi K., Tomlinson, Stephen, Madden, Brian, Bridges, Tracy, Flume, Patrick A., Wrangle, John, Rubinstein, Mark P., Baliga, Prabhakar K., Nadig, Satish N., and Mehrotra, Shikhar

Published
2021
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18. CD38-PyP2 axis-mediated signaling impedes CD8+ T cell response to anti-PD1 therapy in cancer.

Author

Kar, Anwesha, Ghosh, Puspendu, Gautam, Anupam, Chowdhury, Snehanshu, Basak, Debashree, Sarkar, Ishita, Bhoumik, Arpita, Barman, Shubhrajit, Chakraborty, Paramita, Mukhopadhyay, Asima, Mehrotra, Shikhar, Ganesa, Senthil Kumar, Paul, Sandip, and Chatterjee, Shilpak

Subjects
T cells, T-cell exhaustion, T cell differentiation, CANCER treatment, CALCIUM channels
Abstract

PD1 blockade therapy, harnessing the cytotoxic potential of CD8+ T cells, has yielded clinical success in treating malignancies. However, its efficacy is often limited due to the progressive differentiation of intratumoral CD8+ T cells into a hypofunctional state known as terminal exhaustion. Despite identifying CD8+ T cell subsets associated with immunotherapy resistance, the molecular pathway triggering the resistance remains elusive. Given the clear association of CD38 with CD8+ T cell subsets resistant to anti-PD1 therapy, we investigated its role in inducing resistance. Phenotypic and functional characterization, along with single-cell RNA sequencing analysis of both in vitro chronically stimulated and intratumoral CD8+ T cells, revealed that CD38-expressing CD8+ T cells are terminally exhausted. Exploring the molecular mechanism, we found that CD38 expression was crucial in promoting terminal differentiation of CD8+ T cells by suppressing TCF1 expression, thereby rendering them unresponsive to anti-PD1 therapy. Genetic ablation of CD38 in tumor-reactive CD8+ T cells restored TCF1 levels and improved the responsiveness to anti-PD1 therapy in mice. Mechanistically, CD38 expression on exhausted CD8+ T cells elevated intracellular Ca2+ levels through RyR2 calcium channel activation. This, in turn, promoted chronic AKT activation, leading to TCF1 loss. Knockdown of RyR2 or inhibition of AKT in CD8+ T cells maintained TCF1 levels, induced a sustained anti-tumor response, and enhanced responsiveness to anti-PD1 therapy. Thus, targeting CD38 represents a potential strategy to improve the efficacy of anti-PD1 treatment in cancer. [ABSTRACT FROM AUTHOR]

Published
2024
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20. Reviving immunogenic cell death upon targeting TACC3 enhances T-DM1 response in HER2-positive breast cancer

Author

Gedik, Mustafa Emre, primary, Saatci, Ozge, additional, Oberholtzer, Nathaniel, additional, Uner, Meral, additional, Akbulut, Ozge, additional, Cetin, Metin, additional, Aras, Mertkaya, additional, Ibis, Kubra, additional, Caliskan, Burcu, additional, Banoglu, Erden, additional, Wiemann, Stefan, additional, Uner, Aysegul, additional, Aksoy, Sercan, additional, Mehrotra, Shikhar, additional, and Sahin, Ozgur, additional

Published
2023
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22. CD38-NAD+Axis Regulates Immunotherapeutic Anti-Tumor T Cell Response

Author

Chatterjee, Shilpak, Daenthanasanmak, Anusara, Chakraborty, Paramita, Wyatt, Megan W., Dhar, Payal, Selvam, Shanmugam Panneer, Fu, Jianing, Zhang, Jinyu, Nguyen, Hung, Kang, Inhong, Toth, Kyle, Al-Homrani, Mazen, Husain, Mahvash, Beeson, Gyda, Ball, Lauren, Helke, Kristi, Husain, Shahid, Garrett-Mayer, Elizabeth, Hardiman, Gary, Mehrotra, Meenal, Nishimura, Michael I., Beeson, Craig C., Bupp, Melanie Gubbels, Wu, Jennifer, Ogretmen, Besim, Paulos, Chrystal M., Rathmell, Jeffery, Yu, Xue-Zhong, and Mehrotra, Shikhar

Published
2018
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23. Thioredoxin-1 confines T cell alloresponse and pathogenicity in graft-versus-host disease

Author

Sofi, M. Hanief, Wu, Yongxia, Dai, Steven D. SchutMin, Daenthanasanmak, Anusara, Voss, Jessica Heinrichs, Nguyen, Hung, Bastian, David, Selvam, Supinya IamsawaShanmugam Panneer, Liu, Chen, Maulik, Nilanjana, Ogretmen, Besim, Jin, Junfei, Mehrotra, Shikhar, and Yu, Xue-Zhong

Subjects
Bone marrow transplantation -- Analysis -- Health aspects, Cytokines -- Analysis -- Health aspects, Thioredoxins -- Analysis -- Health aspects, Enzymes -- Analysis -- Health aspects, Hematopoietic stem cell transplantation -- Analysis -- Health aspects, Leukemia -- Analysis -- Health aspects, T cells -- Analysis -- Health aspects, Morbidity, Oxidative stress, Surgery, Health care industry, Medical University of South Carolina
Abstract

Oxidative stress is elevated in the recipients of allogeneic hematopoietic cell transplantation (allo-HCT) and likely contributes to the development of graft-versus-host disease (GVHD). GVHD is characterized by activation, expansion, cytokine production, and migration of alloreactive donor T cells, and remains a major cause of morbidity and mortality after allo-HCT. Hence, strategies to limit oxidative stress in GVHD are highly desirable. Thioredoxin-1 (Trx1) counteracts oxidative stress by scavenging ROS and regulating other enzymes that metabolize [H.sub.2][O.sub.2]. The present study sought to elucidate the role of Trx1 in the pathophysiology of GVHD. Using murine and xenograft models of allogeneic bone marrow transplantation (allo-BMT) and genetic (human Trx1-Tg) as well as pharmacological (human recombinant Trx1 [RTrx1]) strategies, we found that Trx1-Tg donor T cells or administration of RTrx1 to the recipients significantly reduced GVHD severity. Mechanistically, we observed that RTrx1 reduced ROS accumulation and cytokine production of mouse and human T cells in response to alloantigen stimulation in vitro. In allo-BMT settings, we found that Trx1-Tg or RTrx1 decreased downstream signaling molecules, including NF-[kappa]B activation and T-bet expression, and reduced proliferation, IFN-[gamma] production, and ROS accumulation in donor T cells within GVHD target organs. More importantly, administration of RTrx1 did not impair the graft-versus-leukemia effect. Taken together, the current work provides a strong rationale for, and demonstrates the feasibility of, targeting the ROS pathway, which can be readily translated to the clinic., Introduction Allogeneic hematopoietic cell transplantation (allo-HCT) is an effective therapeutic procedure to treat hematopoietic malignancy such as leukemia through donor lymphocyte-mediated antitumor response, known as the graft-versus-leukemia (GVL) effect (1, [...]

Published
2019
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24. PIM-2 protein kinase negatively regulates T cell responses in transplantation and tumor immunity

Author

Daenthanasanmak, Anusara, Wu, Yongxia, Nguyen, Supinya IamsawaHung D., Bastian, David, Zhang, MengMeng, Sofi, M. Hanief, Chatterjee, Shilpak, Hill, Elizabeth G., Mehrotra, Shikhar, and Yu, Andrew S. Krafand Xue-Zhong

Subjects
Cell proliferation -- Analysis, T cell antigen receptors -- Research, Protein kinases -- Research, Health care industry
Abstract

PIM kinase family members play a crucial role in promoting cell survival and proliferation via phosphorylation of their target substrates. In this study, we investigated the role of the PIM kinases with respect to T cell responses in transplantation and tumor immunity. We found that the PIM-2 isoform negatively regulated T cell responses to alloantigen, in contrast to the PIM-1 and PIM-3 isoforms, which acted as positive regulators. T cells deficient in PIM-2 demonstrated increased T cell differentiation toward Th1 subset, proliferation, and migration to target organs after allogeneic bone marrow transplantation, resulting in dramatically accelerated graft-versus-host disease (GVHD) severity. Restoration of PIM-2 expression markedly attenuated the pathogenicity of PIM-2-deficient T cells to induce GVHD. On the other hand, mice deficient in PIM-2 readily rejected syngeneic tumor, which was primarily dependent on [CD8.sup.+] T cells. Furthermore, silencing PIM-2 in polyclonal or antigen-specific [CD8.sup.+] T cells substantially enhanced their antitumor response in adoptive T cell immunotherapy. We conclude that PIM-2 kinase plays a prominent role in suppressing T cell responses, and provide a strong rationale to target PIM-2 for cancer immunotherapy., Introduction The provirus integration sites for Moloney murine leukemia virus (PIM) kinases are a highly conserved family of serine/threonine kinases (1, 2). The PIM kinase family is composed of 3 [...]

Published
2018
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32. Data from Enhanced Lymphodepletion Is Insufficient to Replace Exogenous IL2 or IL15 Therapy in Augmenting the Efficacy of Adoptively Transferred Effector CD8+ T Cells

Author

Johnson, C. Bryce, primary, May, Bennett R., primary, Riesenberg, Brian P., primary, Suriano, Samantha, primary, Mehrotra, Shikhar, primary, Garrett-Mayer, Elizabeth, primary, Salem, Mohamed L., primary, Jeng, Emily K., primary, Wong, Hing C., primary, Paulos, Chrystal M., primary, Wrangle, John M., primary, Cole, David J., primary, and Rubinstein, Mark P., primary

Published
2023
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35. Supplementary Data from Targeting PIM Kinase with PD1 Inhibition Improves Immunotherapeutic Antitumor T-cell Response

Author

Chatterjee, Shilpak, primary, Chakraborty, Paramita, primary, Daenthanasanmak, Anusara, primary, Iamsawat, Supinya, primary, Andrejeva, Gabriela, primary, Luevano, Libia A., primary, Wolf, Melissa, primary, Baliga, Uday, primary, Krieg, Carsten, primary, Beeson, Craig C., primary, Mehrotra, Meenal, primary, Hill, Elizabeth G., primary, Rathmell, Jeffery C., primary, Yu, Xue-Zhong, primary, Kraft, Andrew S., primary, and Mehrotra, Shikhar, primary

Published
2023
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36. Supplementary Table from Intracellular Acetyl CoA Potentiates the Therapeutic Efficacy of Antitumor CD8+ T Cells

Author

Chowdhury, Snehanshu, primary, Kar, Anwesha, primary, Bhowmik, Debaleena, primary, Gautam, Anupam, primary, Basak, Debashree, primary, Sarkar, Ishita, primary, Ghosh, Puspendu, primary, Sarkar, Deborpita, primary, Deka, Alvina, primary, Chakraborty, Paramita, primary, Mukhopadhyay, Asima, primary, Mehrotra, Shikhar, primary, Basak, Soumen, primary, Paul, Sandip, primary, and Chatterjee, Shilpak, primary

Published
2023
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38. Data from Carbon Monoxide Activates PERK-Regulated Autophagy to Induce Immunometabolic Reprogramming and Boost Antitumor T-cell Function

Author

Chakraborty, Paramita, primary, Parikh, Rasesh Y., primary, Choi, Seungho, primary, Tran, Danh, primary, Gooz, Monika, primary, Hedley, Zachariah T., primary, Kim, Do-Sung, primary, Pytel, Dariusz, primary, Kang, Inhong, primary, Nadig, Satish N., primary, Beeson, Gyda C., primary, Ball, Lauren, primary, Mehrotra, Meenal, primary, Wang, Hongjun, primary, Berto, Stefano, primary, Palanisamy, Viswanathan, primary, Li, Hong, primary, Chatterjee, Shilpak, primary, Rodriguez, Paulo C., primary, Maldonado, Eduardo N., primary, Diehl, J. Alan, primary, Gangaraju, Vamsi K., primary, and Mehrotra, Shikhar, primary

Published
2023
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39. Supplementary Data from Intracellular Acetyl CoA Potentiates the Therapeutic Efficacy of Antitumor CD8+ T Cells

Author

Chowdhury, Snehanshu, primary, Kar, Anwesha, primary, Bhowmik, Debaleena, primary, Gautam, Anupam, primary, Basak, Debashree, primary, Sarkar, Ishita, primary, Ghosh, Puspendu, primary, Sarkar, Deborpita, primary, Deka, Alvina, primary, Chakraborty, Paramita, primary, Mukhopadhyay, Asima, primary, Mehrotra, Shikhar, primary, Basak, Soumen, primary, Paul, Sandip, primary, and Chatterjee, Shilpak, primary

Published
2023
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40. Supplemental Figures from Enhanced Lymphodepletion Is Insufficient to Replace Exogenous IL2 or IL15 Therapy in Augmenting the Efficacy of Adoptively Transferred Effector CD8+ T Cells

Author

Johnson, C. Bryce, primary, May, Bennett R., primary, Riesenberg, Brian P., primary, Suriano, Samantha, primary, Mehrotra, Shikhar, primary, Garrett-Mayer, Elizabeth, primary, Salem, Mohamed L., primary, Jeng, Emily K., primary, Wong, Hing C., primary, Paulos, Chrystal M., primary, Wrangle, John M., primary, Cole, David J., primary, and Rubinstein, Mark P., primary

Published
2023
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42. Supplementary Figure from Carbon Monoxide Activates PERK-Regulated Autophagy to Induce Immunometabolic Reprogramming and Boost Antitumor T-cell Function

Author

Chakraborty, Paramita, primary, Parikh, Rasesh Y., primary, Choi, Seungho, primary, Tran, Danh, primary, Gooz, Monika, primary, Hedley, Zachariah T., primary, Kim, Do-Sung, primary, Pytel, Dariusz, primary, Kang, Inhong, primary, Nadig, Satish N., primary, Beeson, Gyda C., primary, Ball, Lauren, primary, Mehrotra, Meenal, primary, Wang, Hongjun, primary, Berto, Stefano, primary, Palanisamy, Viswanathan, primary, Li, Hong, primary, Chatterjee, Shilpak, primary, Rodriguez, Paulo C., primary, Maldonado, Eduardo N., primary, Diehl, J. Alan, primary, Gangaraju, Vamsi K., primary, and Mehrotra, Shikhar, primary

Published
2023
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43. Supplementary Figure 4 from Promoting Thiol Expression Increases the Durability of Antitumor T-cell Functions

Author

Kesarwani, Pravin, primary, Al-Khami, Amir A., primary, Scurti, Gina, primary, Thyagarajan, Krishnamurthy, primary, Kaur, Navtej, primary, Husain, Shahid, primary, Fang, Quan, primary, Naga, Osama S., primary, Simms, Patricia, primary, Beeson, Gyda, primary, Voelkel-Johnson, Christina, primary, Garrett-Mayer, Elizabeth, primary, Beeson, Craig C., primary, Nishimura, Michael I., primary, and Mehrotra, Shikhar, primary

Published
2023
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44. Supplementary Figure 2 from Promoting Thiol Expression Increases the Durability of Antitumor T-cell Functions

Author

Kesarwani, Pravin, primary, Al-Khami, Amir A., primary, Scurti, Gina, primary, Thyagarajan, Krishnamurthy, primary, Kaur, Navtej, primary, Husain, Shahid, primary, Fang, Quan, primary, Naga, Osama S., primary, Simms, Patricia, primary, Beeson, Gyda, primary, Voelkel-Johnson, Christina, primary, Garrett-Mayer, Elizabeth, primary, Beeson, Craig C., primary, Nishimura, Michael I., primary, and Mehrotra, Shikhar, primary

Published
2023
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45. Supplementary Material and Methods from Promoting Thiol Expression Increases the Durability of Antitumor T-cell Functions

Author

Kesarwani, Pravin, primary, Al-Khami, Amir A., primary, Scurti, Gina, primary, Thyagarajan, Krishnamurthy, primary, Kaur, Navtej, primary, Husain, Shahid, primary, Fang, Quan, primary, Naga, Osama S., primary, Simms, Patricia, primary, Beeson, Gyda, primary, Voelkel-Johnson, Christina, primary, Garrett-Mayer, Elizabeth, primary, Beeson, Craig C., primary, Nishimura, Michael I., primary, and Mehrotra, Shikhar, primary

Published
2023
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46. Data from Promoting Thiol Expression Increases the Durability of Antitumor T-cell Functions

Author

Kesarwani, Pravin, primary, Al-Khami, Amir A., primary, Scurti, Gina, primary, Thyagarajan, Krishnamurthy, primary, Kaur, Navtej, primary, Husain, Shahid, primary, Fang, Quan, primary, Naga, Osama S., primary, Simms, Patricia, primary, Beeson, Gyda, primary, Voelkel-Johnson, Christina, primary, Garrett-Mayer, Elizabeth, primary, Beeson, Craig C., primary, Nishimura, Michael I., primary, and Mehrotra, Shikhar, primary

Published
2023
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47. Supplementary Figure Legends from Lack of p53 Augments Antitumor Functions in Cytolytic T Cells

Author

Banerjee, Anirban, primary, Thyagarajan, Krishnamurthy, primary, Chatterjee, Shilpak, primary, Chakraborty, Paramita, primary, Kesarwani, Pravin, primary, Soloshchenko, Myroslawa, primary, Al-Hommrani, Mazen, primary, Andrijauskaite, Kristina, primary, Moxley, Kelly, primary, Janakiraman, Harinarayanan, primary, Scheffel, Matthew J., primary, Helke, Kristi, primary, Armenson, Kent, primary, Palanisamy, Viswanathan, primary, Rubinstein, Mark P., primary, Mayer, Elizabeth-Garrett, primary, Cole, David J., primary, Paulos, Chrystal M., primary, Voelkel-Johnson, Christina, primary, Nishimura, Michael I., primary, and Mehrotra, Shikhar, primary

Published
2023
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48. Data from Reducing CD73 Expression by IL1β-Programmed Th17 Cells Improves Immunotherapeutic Control of Tumors

Author

Chatterjee, Shilpak, primary, Thyagarajan, Krishnamurthy, primary, Kesarwani, Pravin, primary, Song, Jin H., primary, Soloshchenko, Myroslawa, primary, Fu, Jianing, primary, Bailey, Stefanie R., primary, Vasu, Chenthamarkshan, primary, Kraft, Andrew S., primary, Paulos, Chrystal M., primary, Yu, Xue-Zhong, primary, and Mehrotra, Shikhar, primary

Published
2023
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49. Supplementary Figures: Lack of p53 Augments Anti-Tumor Functions in Cytolytic T Cells from Lack of p53 Augments Antitumor Functions in Cytolytic T Cells

Author

Banerjee, Anirban, primary, Thyagarajan, Krishnamurthy, primary, Chatterjee, Shilpak, primary, Chakraborty, Paramita, primary, Kesarwani, Pravin, primary, Soloshchenko, Myroslawa, primary, Al-Hommrani, Mazen, primary, Andrijauskaite, Kristina, primary, Moxley, Kelly, primary, Janakiraman, Harinarayanan, primary, Scheffel, Matthew J., primary, Helke, Kristi, primary, Armenson, Kent, primary, Palanisamy, Viswanathan, primary, Rubinstein, Mark P., primary, Mayer, Elizabeth-Garrett, primary, Cole, David J., primary, Paulos, Chrystal M., primary, Voelkel-Johnson, Christina, primary, Nishimura, Michael I., primary, and Mehrotra, Shikhar, primary

Published
2023
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50. Supplementary Figures 1 - 3 from Reducing CD73 Expression by IL1β-Programmed Th17 Cells Improves Immunotherapeutic Control of Tumors

Author

Chatterjee, Shilpak, primary, Thyagarajan, Krishnamurthy, primary, Kesarwani, Pravin, primary, Song, Jin H., primary, Soloshchenko, Myroslawa, primary, Fu, Jianing, primary, Bailey, Stefanie R., primary, Vasu, Chenthamarkshan, primary, Kraft, Andrew S., primary, Paulos, Chrystal M., primary, Yu, Xue-Zhong, primary, and Mehrotra, Shikhar, primary

Published
2023
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