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23 results on '"Long, Kristen B."'

7. TNF blockade uncouples toxicity from antitumor efficacy induced with CD40 chemoimmunotherapy

Author

Stone, Meredith L., primary, Lee, Jesse, additional, Herrera, Veronica M., additional, Graham, Kathleen, additional, Lee, Jae W., additional, Huffman, Austin, additional, Coho, Heather, additional, Tooker, Evan, additional, Myers, Max I., additional, Giannone, Michael, additional, Li, Yan, additional, Buckingham, Thomas H., additional, Long, Kristen B., additional, and Beatty, Gregory L., additional

Published
2021
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10. Interspecies Comparative Genomics Identifies Optimal Mouse Models of Systemic Sclerosis

Author

Sargent, Jennifer L., Li, Zhenghui, Aliprantis, Antonios O., Greenblatt, Matthew, Lemaire, Raphael, Wu, Ming-hua, Wei, Jun, Taroni, Jaclyn, Harris, Adam, Long, Kristen B., Burgwin, Chelsea, Artlett, Carol M., Blankenhorn, Elizabeth P., Lafyatis, Robert, Varga, John, Clark, Stephen H., and Whitfield, Michael L.

Subjects
Male, Disease Models, Animal, Mice, Scleroderma, Systemic, Animals, Humans, Female, Article, Genome-Wide Association Study
Abstract

Understanding the pathogenesis of systemic sclerosis (SSc) is confounded by considerable disease heterogeneity. Animal models of SSc that recapitulate distinct subsets of disease at the molecular level have not been delineated. We applied interspecies comparative analysis of genomic data from multiple mouse models of SSc and patients with SSc to determine which animal models best reflect the SSc intrinsic molecular subsets.Gene expression measured in skin from mice with sclerodermatous graft-versus-host disease (GVHD), bleomycin-induced fibrosis, Tsk1/+ or Tsk2/+ mice was mapped to human orthologs and compared to SSc skin biopsy-derived gene expression. Transforming growth factor β (TGFβ) activation was assessed using a responsive signature in mice, and tumor necrosis factor receptor superfamily member 12A (TNFRSF12A) expression was measured in SSc patient and mouse skin.Gene expression in skin from mice with sclerodermatous GVHD and bleomycin-induced fibrosis corresponded to that in SSc patients in the inflammatory molecular subset. In contrast, Tsk2/+ mice showed gene expression corresponding to the fibroproliferative SSc subset. Enrichment of a TGFβ-responsive signature was observed in both Tsk2/+ mice and mice with bleomycin-induced skin fibrosis. Expression of TNFRSF12A (the TWEAK receptor/fibroblast growth factor-inducible 14) was elevated in skin from patients with fibroproliferative SSc and the skin of Tsk2/+ mice.This study reveals similarities in cutaneous gene expression between distinct mouse models of SSc and specific molecular subsets of the disease. Different pathways underlie the intrinsic subsets including TGFβ, interleukin-13 (IL-13), and IL-4. We identify a novel target, Tnfrsf12a, with elevated expression in skin from patients with fibroproliferative SSc and Tsk2/+ mice. These findings will inform mechanistic and translational preclinical studies in SSc.

Published
2016

12. Abstract IA21: Myeloid cells are required for PD-1/PD-L1 checkpoint activation and the establishment of an immune-suppressive environment in pancreatic cancer

Author

Zhang, Yaqing, primary, Mathew, Esha, additional, Velez-Delgado, Ashley, additional, Long, Kristen B., additional, Li, Dongjun, additional, Mendez, Flor M., additional, Flannagan, Kevin, additional, Rhim, Andrew D., additional, Simeone, Diane M., additional, Beatty, Gregory L., additional, and Magliano, Marina Pasca di, additional

Published
2016
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14. Identification of Optimal Mouse Models of Systemic Sclerosis by Interspecies Comparative Genomics

Author

Sargent, Jennifer L., primary, Li, Zhenghui, additional, Aliprantis, Antonios O., additional, Greenblatt, Matthew, additional, Lemaire, Raphael, additional, Wu, Ming-hua, additional, Wei, Jun, additional, Taroni, Jaclyn, additional, Harris, Adam, additional, Long, Kristen B., additional, Burgwin, Chelsea, additional, Artlett, Carol M., additional, Blankenhorn, Elizabeth P., additional, Lafyatis, Robert, additional, Varga, John, additional, Clark, Stephen H., additional, and Whitfield, Michael L., additional

Published
2016
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17. Exclusion of T Cells From Pancreatic Carcinomas in Mice Is Regulated by Ly6Clow F4/80+ Extratumoral Macrophages

Author

Beatty, Gregory L., primary, Winograd, Rafael, additional, Evans, Rebecca A., additional, Long, Kristen B., additional, Luque, Santiago L., additional, Lee, Jae W., additional, Clendenin, Cynthia, additional, Gladney, Whitney L., additional, Knoblock, Dawson M., additional, Guirnalda, Patrick D., additional, and Vonderheide, Robert H., additional

Published
2015
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19. The Tsk2/+ Mouse Fibrotic Phenotype Is Due to a Gain-of-Function Mutation in the PIIINP Segment of the Col3a1 Gene

Author

Long, Kristen B., primary, Li, Zhenghui, additional, Burgwin, Chelsea M., additional, Choe, Susanna G., additional, Martyanov, Viktor, additional, Sassi-Gaha, Sihem, additional, Earl, Josh P., additional, Eutsey, Rory A., additional, Ahmed, Azad, additional, Ehrlich, Garth D., additional, Artlett, Carol M., additional, Whitfield, Michael L., additional, and Blankenhorn, Elizabeth P., additional

Published
2015
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20. Cancer immunotherapy: activating innate and adaptive immunity through CD40 agonists.

Author

Beatty, Gregory L., Li, Yan, and Long, Kristen B.

Abstract

Introduction: CD40 is a promising therapeutic target for cancer immunotherapy. In patients with advanced solid malignancies, CD40 agonists have demonstrated some anti-tumor activity and a manageable toxicity profile. A 2nd generation of CD40 agonists has now been designed with optimized Fc receptor (FcR) binding based on preclinical evidence suggesting a critical role for FcR engagement in defining the potency of CD40 agonists in vivo. Areas covered: We provide a comprehensive review using PubMed and Google Patent databases on the current clinical status of CD40 agonists, strategies for applying CD40 agonists in cancer therapy, and the preclinical data that supports and is guiding the future development of CD40 agonists. Expert commentary: There is a wealth of preclinical data that provide rationale on several distinct approaches for using CD40 agonists in cancer immunotherapy. This data illustrates the need to strategically combine CD40 agonists with other clinically active treatment regimens in order to realize the full potential of activating CD40 in vivo. Thus, critical to the success of this class of immune-oncology drugs, which have the potential to restore both innate and adaptive immunosurveillance, will be the identification of biomarkers for monitoring and predicting responses as well as informing mechanisms of treatment resistance. [ABSTRACT FROM AUTHOR]

Published
2017
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