About

Ana María León Crespo is an Associate Professor of Architecture at Harvard Graduate School of Design. Her work traces how spatial practices and transnational networks of power and resistance shape the modernity and coloniality of the Americas. Her research and teaching foreground the agency of populations under struggle and the multiple forms of bias embedded in the built environment and its histories. León is invested in collaborative approaches to learning, teaching, and writing, emphasizing the importance of multiple critical positions, particularly those of historically underrepresented groups, to ground understanding of history in the politics of coliberation. She is the author of 'Modernity for the Masses: Antonio Bonet’s Dreams for Buenos Aires' (University of Texas Press, 2021) and 'A Ruin in Reverse / Bones of the Nation' (ARQ, 2021). León has edited issues of academic journals such as Thresholds, The Architectural Theory Review, and e-flux Architecture, and her writing has been published in multiple journals and anthologies. She has organized actions at major art and architecture events, including the Venice Biennale and the Chicago Architecture Biennial, and has co-organized teaching workshops on feminist pedagogy, settler colonialism, and anti-racism in architectural history. Prior to her current position, she was Assistant Professor at the University of Michigan. She holds a Ph.D. in the History, Theory, and Criticism of Architecture from MIT, a Master in Design Studies with distinction from the GSD, a Master in Architecture from Georgia Tech, and a diploma in architecture from UCSG Ecuador. León serves on the editorial board of several journals and has been involved in various boards and collectives aimed at broadening the reach of architectural history, including the Feminist Art and Architecture Collaborative, Detroit Resists, Nuestro Norte es el Sur, and the Settler Colonial City Project. Additional information and links are available at anamarialeon.net.

Research topics

• Immunology
• Biology
• Virology
• Medicine
• Cell biology
• Biochemistry

Selected publications

• UNA SIMPLE CONJUNTIVITIS PUEDE SER UN PROBLEMA SOCIAL

  2025-06-26

  article
  PublisherDOI

• ANÁLISIS CLÍNICO Y ANALÍTICO DE LAS INFECCIONES DEL TRACTO URINARIO CAUSADAS POR ENTEROCOCO FAECALIS

  2025-06-26

  article
  PublisherDOI

• The NK cell receptor NKp46 recognizes ecto-calreticulin on ER-stressed cells

  Nature · 2023-04-05 · 170 citations

  articleOpen access
  PublisherOA PDFDOI

• Publisher Correction: The NK cell receptor NKp46 recognizes ecto-calreticulin on ER-stressed cells

  Nature · 2023-05-17 · 8 citations

  erratumOpen access
  PublisherOA PDFDOI

• FcγR-mediated SARS-CoV-2 infection of monocytes activates inflammation

  Nature · 2022 · 573 citations

  • Immunology
  • Biology
  • Virology
  PublisherOA PDFDOI

• Mesenchymal and adrenergic cell lineage states in neuroblastoma possess distinct immunogenic phenotypes

  Nature Cancer · 2022-09-22 · 85 citations

  articleOpen access
  PublisherOA PDFDOI

• Purification of Primary Decidual Natural Killer Cells for Functional Analysis

  Methods in molecular biology · 2022-01-01 · 2 citations

  article1st author
  PublisherDOI

• Abstract A08: Divergent tumor cell states in neuroblastoma possess distinct immunogenic phenotypes

  Cancer Immunology Research · 2022-12-01

  article

  Abstract Active immunotherapy approaches for neuroblastoma (NB), a pediatric cancer of the sympathetic nervous system, has met with limited success. Especially challenging is the genetic heterogeneity of NB which makes it difficult to identify factors that consistently indicate the likelihood of an effective immune response and thereby select patients who are most likely to benefit from immunotherapy. Hence, we undertook an unbiased analysis of gene expression signatures from >500 well-annotated primary NBs representing diverse clinical and genetic subtypes to identify of predictors of immune response. Using clustering analysis of bulk transcriptomic signatures from these tumors, we identified a subset of NBs that was notable for the high expression of genes associated with anti-tumor immune response. These “immunogenic” tumors showed a predominance of gene expression signatures derived from malignant cells with primitive neural crest-like or mesenchymal properties, one of the two cell states that shape intratumoral heterogeneity in NB. In contrast, tumors that expressed committed, adrenergic neuron-like signatures were less immunogenic. Single-cell (sc) RNA-seq and immunohistochemistry analysis further confirmed that NBs comprise both adrenergic and mesenchymal tumor cells, and that the presence of mesenchymal cells positively associated with immune cell infiltration into the TME. scRNA-seq also revealed that mesenchymal NB cells were enriched for inflammatory gene signature. Gene expression analysis of isogenic pairs of adrenergic and mesenchymal cells showed that mesenchymal NBs differentially upregulate genes involved in regulating antigen processing and presentation, MHC class I expression, type-I interferon and TLR3 signaling, and NK cell activation. This is achieved through a permissive chromatin landscape at the promoters of these immune regulatory genes that support their high expression in mesenchymal cells. By contrast, in adrenergic cells, tumor-intrinsic immune genes are epigenetically silenced by the PRC2 complex and PRC2 inhibition leads to increased immune cell activation. Remarkably, induction of the mesenchymal state in adrenergic cells through transcriptional reprogramming by PRRX1 or therapy resistance is accompanied by the epigenetic activation of innate and adaptive immune response genes. Functionally, the inherent immunogenicity of mesenchymal cells promotes T cell infiltration by secreting inflammatory cytokines, enables efficient targeting by antigen-specific cytotoxic T and NK cells, and imparts responsiveness to immune checkpoint blockade in a syngeneic NB model. In conclusion, our study uncovers an unappreciated link between immunogenicity and tumor lineage state in NB, and rationalizes future interrogations into (i) avenues through which the vulnerability of mesenchymal cells to immune-mediated targeting could be harnessed clinically and (ii) how perturbation of epigenetically-regulated cell states could be harnessed to promote anti-tumor immune response. Citation Format: Satyaki Sengupta, Sanjukta Das, Angela C. Crespo, Annelisa M. Cornel, Anand G. Patel, Navin R. Mahadevan, Marco Campisi, Alaa K. Ali, Bandana Sharma, Jared H. Rowe, Rogier Versteeg, Rudolf Jaenisch, Stefani Spranger, Rizwan Romee, Brian C. Miller, David A. Barbie, Stefan Nierkens, Michael A. Dyer, Judy Lieberman, Rani E. George. Divergent tumor cell states in neuroblastoma possess distinct immunogenic phenotypes [abstract]. In: Proceedings of the AACR Special Conference: Tumor Immunology and Immunotherapy; 2022 Oct 21-24; Boston, MA. Philadelphia (PA): AACR; Cancer Immunol Res 2022;10(12 Suppl):Abstract nr A08.

  PublisherDOI

• Decidual NK cells kill Zika virus–infected trophoblasts

  Proceedings of the National Academy of Sciences · 2021-11-16 · 31 citations

  articleOpen access

  Significance Natural killer cells (NK) defend against viruses. Decidual NK (dNK), which comprise ∼70% of decidual leukocytes during early pregnancy, are poorly cytotoxic but promote placentation. Zika virus (ZIKV) can cause fetal loss and birth defects. A strong dNK-mediated antiviral defense could provide a barrier to placental infections. Here, we show that ZIKV infection transforms immune-tolerated trophoblasts into dNK targets because ZIKV replicates in the endoplasmic reticulum (ER) and causes ER stress, which triggers NK killing. Unlike in the case of other viral infections, dNK release their granules and kill ZIKV-infected trophoblasts. In a trophoblast-like cell line, human primary extravillous trophoblasts, 3D villous explants, and Ifnar1 −/− pregnant mice, dNK reduce placental and fetal viral loads and protect against fetal loss.

  PublisherOA PDFDOI

• SARS-CoV-2 infects blood monocytes to activate NLRP3 and AIM2 inflammasomes, pyroptosis and cytokine release

  Research Square (Research Square) · 2021 · 74 citations

  • Immunology
  • Biology
  • Virology

  SARS-CoV-2 causes acute respiratory distress that can progress to multiorgan failure and death in a minority of patients. Although severe COVID-19 disease is linked to exuberant inflammation, how SARS-CoV-2 triggers inflammation is not understood. Monocytes and macrophages are sentinel immune cells in the blood and tissue, respectively, that sense invasive infection to form inflammasomes that activate caspase-1 and gasdermin D (GSDMD) pores, leading to inflammatory death (pyroptosis) and processing and release of IL-1 family cytokines, potent inflammatory mediators. Here we show that expression quantitative trait loci (eQTLs) linked to higher GSDMD expression increase the risk of severe COVID-19 disease (odds ratio, 1.3, p<0.005). We find that about 10% of blood monocytes in COVID-19 patients are infected with SARS-CoV-2. Monocyte infection depends on viral antibody opsonization and uptake of opsonized virus by the Fc receptor CD16. After uptake, SARS-CoV-2 begins to replicate in monocytes, as evidenced by detection of double-stranded RNA and subgenomic RNA and expression of a fluorescent reporter gene. However, infection is aborted, and infectious virus is not detected in infected monocyte supernatants or patient plasma. Instead, infected cells undergo inflammatory cell death (pyroptosis) mediated by activation of the NLRP3 and AIM2 inflammasomes, caspase-1 and GSDMD. Moreover, tissue-resident macrophages, but not infected epithelial cells, from COVID-19 lung autopsy specimens showed evidence of inflammasome activation. These findings taken together suggest that antibody-mediated SARS-CoV-2 infection of monocytes/macrophages triggers inflammatory cell death that aborts production of infectious virus but causes systemic inflammation that contributes to severe COVID-19 disease pathogenesis.

  PublisherOA PDFDOI

Frequent coauthors

• Judy Lieberman

  Harvard University

  34 shared

• Tamara Tilburgs

  Cincinnati Children's Hospital Medical Center

  29 shared

• Caroline Junqueira

  Fundação Oswaldo Cruz

  28 shared

• Jack L. Strominger

  Harvard University

  23 shared

• Luciana Costa

  Fundação Oswaldo Cruz

  17 shared

• Madalena Martins

  Hospital Santo António dos Capuchos

  16 shared

• Sumit Sen Santara

  16 shared

• Hao Wu

  Harvard University

  14 shared

Education

• Ph.D., Architecture

  Harvard University

  2009

• M.A., Architecture

  Harvard University

  2004

• B.A., Architecture

  University of California, Berkeley

  2001