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19 results on '"Hartigan, Adam J."'

1. Engineered Stem Cell Antibody Paired Evasion 1 (ESCAPE-1): Paired HSC Epitope Engineering and Upregulation of Fetal Hemoglobin for Antibody-Mediated Autologous Hematopoietic Stem Cell Therapy Conditioning for the Treatment of Hemoglobinopathies

Author

Mondal, Nandini, primary, Harmon, Alexander, additional, Budak, Elizabeth, additional, Zhang, Kathy, additional, Wong, Jeffrey, additional, Rinaldi, Conrad, additional, Olins, Jenny, additional, Hoar, Kara, additional, Menon, Archita Venugopal, additional, White, Moriah, additional, Musenge, Faith, additional, Camblin, Adam, additional, Wolin, Adam, additional, Coisman, Brent, additional, Bai, Tao, additional, Qiao, Kangjian, additional, Patel, Mudra, additional, Decker, Jeremy, additional, Gantzer, Bob, additional, Leete, Thomas, additional, Yu, Yi, additional, Bohnuud, Tanggis, additional, Lee, Seung-Joo, additional, Smith, Sarah, additional, McDonagh, Charlotte F, additional, Gaudelli, Nicole M., additional, Chu, S. Haihua, additional, Hartigan, Adam J., additional, and Ciaramella, Giuseppe, additional

Published
2022
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2. Engineered Stem Cell Antibody Paired Evasion-2 (ESCAPE-2): Paired HSC Epitope Engineering and Direct Editing of Sickle Allele for Antibody-Mediated Autologous Hematopoietic Stem Cell Therapy Conditioning for the Treatment of Sickle Cell Disease

Author

Chu, S. Haihua, primary, Budak, Elizabeth, additional, Mondal, Nandini, additional, Zhang, Kathy, additional, Harmon, Alexander, additional, Wong, Jeffrey, additional, Lam, Dieter, additional, Lucini, Corrina, additional, Coisman, Brent, additional, Qiao, Kangjian, additional, Bai, Tao, additional, Decker, Jeremy, additional, Gantzer, Bob, additional, Lee, Kindo, additional, Sen, Maya, additional, Bohnuud, Tanggis, additional, Barrera, Luis, additional, Cafferty, Brian, additional, Lee, Seung-Joo, additional, Kopesky, Paul, additional, Gaudelli, Nicole M., additional, McDonagh, Charlotte F, additional, Ciaramella, Giuseppe, additional, and Hartigan, Adam J., additional

Published
2022
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4. Conversion of HbS to Hb G-Makassar By Adenine Base Editing Is Compatible with Normal Hemoglobin Function

Author

Chu, S. Haihua, primary, Ortega, Manuel, additional, Feliciano, Paty, additional, Winton, Valerie, additional, Xu, Chavonna, additional, Haupt, Daniel, additional, McDonald, Teresa, additional, Martinez, Salette, additional, Liquori, Alexander, additional, Marshall, Jeffrey, additional, Lam, Daisy, additional, Olins, Jenny, additional, Rinaldi, Conrad, additional, Rehberger, Kyle, additional, Lazarra, Colin, additional, Decker, Jeremy, additional, Gantzer, Bob, additional, Bohnuud, Tanggis, additional, Born, David, additional, Barrera, Luis, additional, Yan, Bo, additional, Slaymaker, Ian, additional, Packer, Michael S., additional, Smith, Sarah, additional, Zambonelli, Carlo, additional, Lee, Matt, additional, Gaudelli, Nicole M., additional, Hartigan, Adam J., additional, and Ciaramella, Giuseppe, additional

Published
2021
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5. Adenine Base Editing of the Sickle Allele in CD34+ Hematopoietic Stem and Progenitor Cells Eliminates Hemoglobin S

Author

Chu, S. Haihua, primary, Lam, Daisy, additional, Packer, Michael S., additional, Olins, Jennifer, additional, Liquori, Alexander, additional, Marshall, Jeffrey, additional, Lee, Calvin, additional, Yan, Bo, additional, Decker, Jeremy, additional, Gantzer, Bob, additional, Haskett, Scott J., additional, Bohnuud, Tanggis, additional, Born, David, additional, Barrera, Luis, additional, Slaymaker, Ian, additional, Gaudelli, Nicole M., additional, Hartigan, Adam J., additional, and Ciaramella, Giuseppe, additional

Published
2020
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6. Interleukin-33 contributes to both M1 and M2 chemokine marker expression in human macrophages

Author

Kunkel Steven L, Finn William G, Hartigan Adam J, Oak Sameer R, Joshi Amrita D, Duffy Karen E, Das Anuk, and Hogaboam Cory M

Subjects
Immunologic diseases. Allergy, RC581-607
Abstract

Abstract Background Interleukin-33 is a member of the IL-1 cytokine family whose functions are mediated and modulated by the ST2 receptor. IL-33-ST2 expression and interactions have been explored in mouse macrophages but little is known about the effect of IL-33 on human macrophages. The expression of ST2 transcript and protein levels, and IL-33-mediated effects on M1 (i.e. classical activation) and M2 (i.e. alternative activation) chemokine marker expression in human bone marrow-derived macrophages were examined. Results Human macrophages constitutively expressed the membrane-associated (i.e. ST2L) and the soluble (i.e. sST2) ST2 receptors. M2 (IL-4 + IL-13) skewing stimuli markedly increased the expression of ST2L, but neither polarizing cytokine treatment promoted the release of sST2 from these cells. When added to naïve macrophages alone, IL-33 directly enhanced the expression of CCL3. In combination with LPS, IL-33 blocked the expression of the M2 chemokine marker CCL18, but did not alter CCL3 expression in these naive cells. The addition of IL-33 to M1 macrophages markedly increased the expression of CCL18 above that detected in untreated M1 macrophages. Similarly, alternatively activated human macrophages treated with IL-33 exhibited enhanced expression of CCL18 and the M2 marker mannose receptor above that detected in M2 macrophages alone. Conclusions Together, these data suggest that primary responses to IL-33 in bone marrow derived human macrophages favors M1 chemokine generation while its addition to polarized human macrophages promotes or amplifies M2 chemokine expression.

Published
2010
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8. A Non-Genotoxic Antibody Drug Conjugate Targeting C-Kit for Hematopoietic Stem Cell Transplant Conditioning

Author

Hartigan, Adam J., primary, Pearse, Brad R., additional, McDonough, Sean M., additional, Proctor, Jennifer L., additional, Adams, Hillary L., additional, McShea, Molly A., additional, Hoban, Megan D., additional, Panwar, Rajiv, additional, Hyzy, Sharon L., additional, Goncalves, Kevin A., additional, Palchaudhuri, Rahul, additional, Boitano, Anthony E., additional, and Cooke, Michael P., additional

Published
2018
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11. Growth Differentiation Factor 11 Is a Circulating Factor that Reverses Age-Related Cardiac Hypertrophy

Author

Loffredo, Francesco S., primary, Steinhauser, Matthew L., additional, Jay, Steven M., additional, Gannon, Joseph, additional, Pancoast, James R., additional, Yalamanchi, Pratyusha, additional, Sinha, Manisha, additional, Dall’Osso, Claudia, additional, Khong, Danika, additional, Shadrach, Jennifer L., additional, Miller, Christine M., additional, Singer, Britta S., additional, Stewart, Alex, additional, Psychogios, Nikolaos, additional, Gerszten, Robert E., additional, Hartigan, Adam J., additional, Kim, Mi-Jeong, additional, Serwold, Thomas, additional, Wagers, Amy J., additional, and Lee, Richard T., additional

Published
2013
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17. T regulatory cells and attenuated bleomycininduced fibrosis in lungs of CCR7-/- mice.

Author

Trujillo, Glenda, Hartigan, Adam J., and Hogaboam, Cory M.

Subjects
*CHEMOKINES, *DENDRITIC cells, *CELL migration, *WOUND healing, *TISSUES, *PULMONARY fibrosis, *BLEOMYCIN, *COLLAGEN, *LYMPHOID tissue
Abstract

Background: C-C chemokine receptor (CCR)7 is a regulator of dendritic cell and T cell migration, and its role in tissue wound healing has been investigated in various disease models. We have previously demonstrated that CCR7 and its ligand, chemokine (C-C motif) ligand (CCL)21, modulates wound repair in pulmonary fibrosis (PF) but the mechanism of this is unknown. The objective of this study was to investigate whether the absence of CCR7 protects against bleomycin (BLM)-induced PF. CCR7-/- mice failed to mount a fibrotic pulmonary response as assessed by histologic collagen staining and quantification by hydroxyproline. We hypothesized that the prominent characteristics of CCR7-/- mice, including elevated levels of cytokine and chemokine mediators and the presence of bronchus-associated lymphoid tissue (BALT) might be relevant to the protective phenotype. Results: Pulmonary fibrosis was induced in CCR7+/+ and CCR7-/- mice via a single intratracheal injection of BLM. We found that the lung cytokine/chemokine milieu associated with the absence of CCR7 correlated with an increase in BALT, and might be attributable to regulatory T cell (Treg) homeostasis and trafficking within the lungs and lymph nodes. In response to BLM challenge, CCR7-/- mice exhibited an early, steady increase in lung CD4+ T cells and increased CD4+ CD25+ FoxP3+ Tregs in the lungs 21 days after challenge. These findings are consistent with increased lung expression of interleukin-2 and indoleamine 2,3-dioxygenase in CCR7-/- mice, which promote Treg expansion. Conclusions: Our study demonstrates that the protective phenotype associated with BLM-treated CCR7-/- mice correlates with the presence of BALT and the anchoring of Tregs in the lungs of CCR7-/- mice. These data provide novel evidence to support the further investigation of CCR7-mediated Treg trafficking in the modulation of BLMinduced PF. [ABSTRACT FROM AUTHOR]

Published
2010
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18. Adenine Base Editing of the Sickle Allele in CD34+Hematopoietic Stem and Progenitor Cells Eliminates Hemoglobin S

Author

Chu, S. Haihua, Lam, Daisy, Packer, Michael S., Olins, Jennifer, Liquori, Alexander, Marshall, Jeffrey, Lee, Calvin, Yan, Bo, Decker, Jeremy, Gantzer, Bob, Haskett, Scott J., Bohnuud, Tanggis, Born, David, Barrera, Luis, Slaymaker, Ian, Gaudelli, Nicole M., Hartigan, Adam J., and Ciaramella, Giuseppe

Abstract

While there are several small molecule, gene therapy, and gene editing approaches for treating sickle cell disease (SCD), these strategies do not result in the direct elimination of the causative sickle β-globin (HbS) variant itself. The reduction or complete removal of this pathologic globin variant and expression of normal β-hemoglobin (HbB) or other non-polymerizing β-globin variant may increase the likelihood of beneficial outcomes for SCD patients. Adenine base editors (ABEs) can precisely convert the mutant A-T base pair responsible for SCD to a G-C base pair, thus generating the hemoglobin variant, Hb G-Makassar, a naturally occurring β-globin variant that is not associated with human disease.

Published
2020
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19. Growth Differentiation Factor 11 is a Circulating Factor that Reverses Age-Related Cardiac Hypertrophy

Author

Amy J. Wagers, Alex Stewart, Matthew L. Steinhauser, Joseph Gannon, Nikolaos Psychogios, Danika Mei Po Khong, Christine M. Miller, Manisha Sinha, Adam J. Hartigan, Steven M. Jay, Claudia Dall'Osso, Mi-Jeong Kim, Pratyusha Yalamanchi, J Shadrach, Richard T. Lee, Francesco S. Loffredo, Thomas Serwold, Robert E. Gerszten, James R. Pancoast, Britta Singer, Loffredo, Francesco S., Steinhauser, Matthew L., Jay, Steven M., Gannon, Joseph, Pancoast, James R., Yalamanchi, Pratyusha, Sinha, Manisha, Dall'Osso, Claudia, Khong, Danika, Shadrach, Jennifer L., Miller, Christine M., Singer, Britta S., Stewart, Alex, Psychogios, Nikolao, Gerszten, Robert E., Hartigan, Adam J., Kim, Mi-Jeong, Serwold, Thoma, Wagers, Amy J., and Lee, Richard T.

Subjects
Male, medicine.medical_specialty, Aging, Parabiosis, Induced Pluripotent Stem Cells, Blood Pressure, Cardiomegaly, Biology, General Biochemistry, Genetics and Molecular Biology, Induced Pluripotent Stem Cell, Article, Muscle hypertrophy, Mice, Internal medicine, medicine, Myocyte, Animals, Humans, Myocytes, Cardiac, Biochemistry, Genetics and Molecular Biology (all), Animal, Biochemistry, Genetics and Molecular Biology(all), Bone Morphogenetic Protein, Growth differentiation factor, Forkhead Transcription Factors, Forkhead Transcription Factor, medicine.disease, Mice, Inbred C57BL, Growth Differentiation Factors, Endocrinology, Blood pressure, Growth Differentiation Factor, Heart failure, GDF11, Bone Morphogenetic Proteins, Hypertrophy, Left Ventricular, Female, Parabiosi, Transforming growth factor, Human
Abstract

SummaryThe most common form of heart failure occurs with normal systolic function and often involves cardiac hypertrophy in the elderly. To clarify the biological mechanisms that drive cardiac hypertrophy in aging, we tested the influence of circulating factors using heterochronic parabiosis, a surgical technique in which joining of animals of different ages leads to a shared circulation. After 4 weeks of exposure to the circulation of young mice, cardiac hypertrophy in old mice dramatically regressed, accompanied by reduced cardiomyocyte size and molecular remodeling. Reversal of age-related hypertrophy was not attributable to hemodynamic or behavioral effects of parabiosis, implicating a blood-borne factor. Using modified aptamer-based proteomics, we identified the TGF-β superfamily member GDF11 as a circulating factor in young mice that declines with age. Treatment of old mice to restore GDF11 to youthful levels recapitulated the effects of parabiosis and reversed age-related hypertrophy, revealing a therapeutic opportunity for cardiac aging.PaperFlick

Published
2013

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