Professional Education

  • Doctor of Philosophy (Ph.D.), Oklahoma State University Center for Health Sciences, Immunology (2019)
  • Master of Science, VIT University, India, Biomedical Genetics (2014)
  • Bachelor of Technology, SRM University, India, Genetic Engineering (2011)

Stanford Advisors

All Publications

  • Application of Mass Cytometry Platforms to Solid Organ Transplantation. Transplantation Zhang, W., Sen, A., Pena, J. K., Reitsma, A., Alexander, O. C., Tajima, T., Martinez, O. M., Krams, S. M. 2024


    Transplantation serves as the cornerstone of treatment for patients with end-stage organ disease. The prevalence of complications, such as allograft rejection, infection, and malignancies, underscores the need to dissect the complex interactions of the immune system at the single-cell level. In this review, we discuss studies using mass cytometry or cytometry by time-of-flight, a cutting-edge technology enabling the characterization of immune populations and cell-to-cell interactions in granular detail. We review the application of mass cytometry in human and experimental animal studies in the context of transplantation, uncovering invaluable contributions of the tool to understanding rejection and other transplant-related complications. We discuss recent innovations that have the potential to streamline and standardize mass cytometry workflows for application to multisite clinical trials. Additionally, we introduce imaging mass cytometry, a technique that couples the power of mass cytometry with spatial context, thereby mapping cellular interactions within tissue microenvironments. The synergistic integration of mass cytometry and imaging mass cytometry data with other omics data sets and high-dimensional data platforms to further define immune dynamics is discussed. In conclusion, mass cytometry technologies, when integrated with other tools and data, shed light on the intricate landscape of the immune response in transplantation. This approach holds significant potential for enhancing patient outcomes by advancing our understanding and facilitating the development of new diagnostics and therapeutics.

    View details for DOI 10.1097/TP.0000000000004925

    View details for PubMedID 38467594

  • Extracellular vesicle microRNAs are decreased in pediatric solid-organ transplant recipients during EBV plus post-transplant lymphoproliferative disorder Sen, A., Enriquez, J., Rao, M., Esquivel, C. O., Martinez, O. M., Krams, S. M. WILEY. 2023
  • Host microRNAs are decreased in pediatric solid-organ transplant recipients during EBV+ Post-transplant Lymphoproliferative Disorder. Frontiers in immunology Sen, A., Enriquez, J., Rao, M., Glass, M., Balachandran, Y., Syed, S., Twist, C. J., Weinberg, K., Boyd, S. D., Bernstein, D., Trickey, A. W., Gratzinger, D., Tan, B., Lapasaran, M. G., Robien, M. A., Brown, M., Armstrong, B., Desai, D., Mazariegos, G., Chin, C., Fishbein, T. M., Venick, R. S., Tekin, A., Zimmermann, H., Trappe, R. U., Anagnostopoulos, I., Esquivel, C. O., Martinez, O. M., Krams, S. M. 2022; 13: 994552


    Post-transplant lymphoproliferative disorder (PTLD) is a serious complication of solid organ transplantation. Predisposing factors include primary Epstein-Barr virus (EBV) infection, reactivation of EBV in recipient B cells, and decreased T cell immunity due to immunosuppression. In our previous studies EBV infection was demonstrated to markedly alter the expression of host B cell microRNA (miR). Specifically, miR-194 expression was uniquely suppressed in EBV+ B cell lines from PTLD patients and the 3'untranslated region of IL-10 was determined to be targeted by miR-194. Although EBV has been shown to regulate host miR expression in B cell lymphoma cell lines, the expression of miRs in the circulation of patients with EBV-associated PTLD has not been studied. The objective of this study was to determine if changes in miR expression are associated with EBV+ PTLD. In this study, we have shown that miR-194 is significantly decreased in EBV+PTLD tumors and that additional miRs, including miRs-17, 19 and 106a are also reduced in EBV+PTLD as compared to EBV-PTLD. We quantitated the levels of miRs-17, 19, 106a, 155, and 194 in the plasma and extracellular vesicles (EV; 50-70 nm as determined by nanoparticle tracking analysis) from pediatric recipients of solid organ transplants with EBV+ PTLD+ that were matched 1:2 with EBV+ PTLD- pediatric transplant recipients as part of the NIH-sponsored Clinical Trials in Organ Transplantation in Children, (CTOTC-06) study. Levels of miRs-17, 19, 106a, and 194 were reduced in the plasma and extracellular vesicles (EV) of EBV+ PTLD+ group compared to matched controls, with miRs-17 (p = 0.034; plasma), miRs-19 (p = 0.029; EV) and miR-106a (p = 0.007; plasma and EV) being significantly reduced. Similar levels of miR-155 were detected in the plasma and EV of all pediatric SOT recipients. Importantly, ~90% of the cell-free miR were contained within the EV supporting that EBV+ PTLD tumor miR are detected in the circulation and suggesting that EVs, containing miRs, may have the potential to target and regulate cells of the immune system. Further development of diagnostic, mechanistic and potential therapeutic uses of the miRs in PTLD is warranted.

    View details for DOI 10.3389/fimmu.2022.994552

    View details for PubMedID 36304469

  • Estrogen receptors in human bladder cells regulate innate cytokine responses to differentially modulate uropathogenic E. coli colonization. Immunobiology Sen, A. n., Kaul, A. n., Kaul, R. n. 2020; 226 (1): 152020


    The bladder epithelial cells elicit robust innate immune responses against urinary tract infections (UTIs) for preventing the bacterial colonization. Physiological fluctuations in circulating estrogen levels in women increase the susceptibility to UTI pathogenesis, often resulting in adverse health outcomes. Dr adhesin bearing Escherichia coli (Dr E. coli) cause recurrent UTIs in menopausal women and acute pyelonephritis in pregnant women. Dr E. coli bind to epithelial cells via host innate immune receptor CD55, under hormonal influence. The role of estrogens or estrogen receptors (ERs) in regulating the innate immune responses in the bladder are poorly understood. In the current study, we investigated the role of ERα, ERβ and GPR30 in modulating the innate immune responses against Dr E. coli induced UTI using human bladder epithelial carcinoma 5637 cells (HBEC). Both ERα and ERβ agonist treatment in bladder cells induced a protection against Dr E. coli invasion via upregulation of TNFα and downregulation of CD55 and IL10, and these effects were reversed by action of ERα and ERβ antagoinsts. In contrast, the agonist-mediated activation of GPR30 led to an increased bacterial colonization due to suppression of innate immune factors in the bladder cells, and these effects were reversed by the antagonist-mediated suppression of GPR30. Further, siRNA-mediated ERα knockdown in the bladder cells reversed the protection against bacterial invasion observed in the ERα positive bladder cells, by modulating the gene expression of TNFα, CD55 and IL10, thus confirming the protective role of ERα. We demonstrate for the first time a protective role of nuclear ERs, ERα and ERβ but not of membrane ER, GPR30 against Dr E. coli invasion in HBEC 5637 cells. These findings have many clinical implications and suggest that ERs may serve as potential drug targets towards developing novel therapeutics for regulating local innate immunity and treating UTIs.

    View details for DOI 10.1016/j.imbio.2020.152020

    View details for PubMedID 33246308

  • Estrogen receptor alpha differentially modulates host immunity in the bladder and kidney in response to urinary tract infection AMERICAN JOURNAL OF CLINICAL AND EXPERIMENTAL UROLOGY Sen, A., Iyer, J., Boddu, S., Kaul, A., Kaul, R. 2019; 7 (3): 110–22


    The protective role of endogenous estrogen against Urinary Tract Infection (UTI) is well recognized, but the involvement of estrogen receptors (ERs) in modulating immunity in the urinary tract during UTI pathogenesis has not been investigated. The current study investigates the role of ERα in modulating immune responses and UTI outcome. Mice were pre-treated with either ERα agonist, propyl-pyrazole-triol (PPT), or ERα antagonist, methyl-piperidino-pyrazole (MPP), before experimental UTI. The UTI outcome was determined by checking the bacterial load, CD55 and TNFα expression in the bladder and kidney tissues. We observed opposite effects of PPT and MPP treatment on bacterial clearance in bladder versus kidney. PPT significantly reduced bacterial load (P < 0.05) only in the kidney, with minimal changes in CD55 and TNFα levels. In contrast, MPP showed remarkable bacterial clearance only in the bladder that corresponded with reduced CD55 and TNFα expression. MPP treatment in uninfected state induced a significant increase in TNFα production (P < 0.05) in the bladder, but not in the kidney. Our results suggest a protective role of ERα in the kidney. However, protection in the bladder may be mediated via other ER subtypes that may be involved in boosting the local immune responses. Drugs targeting specific ERs in bladder may serve as an adjunct treatment for boosting immune responses in the urogenital tract for efficient bacterial clearance.

    View details for Web of Science ID 000473314700002

    View details for PubMedID 31317051

    View details for PubMedCentralID PMC6627544