8 results on '"Adams, Taylor"'
Search Results
2. VISTA (PD-1H) Is a Crucial Immune Regulator to Limit Pulmonary Fibrosis
- Author
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Kim, Sang-Hun, primary, Adams, Taylor S, additional, Hu, Qianni, additional, Shin, Hyeon Jun, additional, Chae, Ganghee, additional, Lee, Sang Eun, additional, Sharma, Lokesh, additional, Kwon, Hyuk-Kwon, additional, Lee, Francis Y, additional, Park, Hong-Jai, additional, Huh, Won Jae, additional, Manning, Edward, additional, Kaminski, Naftali, additional, Sauler, Maor, additional, Chen, Lieping, additional, Song, Jin Woo, additional, Kim, Tae Kon, additional, and Kang, Min-Jong, additional
- Published
- 2022
- Full Text
- View/download PDF
3. CD38 Mediates Lung Fibrosis by Promoting Alveolar Epithelial Cell Aging
- Author
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Cui, Huachun, primary, Xie, Na, additional, Banerjee, Sami, additional, Dey, Tapan, additional, Liu, Rui-Ming, additional, Antony, Veena B., additional, Sanders, Yan Y., additional, Adams, Taylor S., additional, Gomez, Jose L., additional, Thannickal, Victor J., additional, Kaminski, Naftali, additional, and Liu, Gang, additional
- Published
- 2022
- Full Text
- View/download PDF
4. VISTA (PD-1H) Is a Crucial Immune Regulator to Limit Pulmonary Fibrosis.
- Author
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Sang-Hun Kim, Adams, Taylor S., Qianni Hu, Hyeon Jun Shin, Ganghee Chae, Sang Eun Lee, Sharma, Lokesh, Hyuk-Kwon Kwon, Lee, Francis Y., Hong-Jai Park, Won Jae Huh, Manning, Edward, Kaminski, Naftali, Sauler, Maor, Lieping Chen, Jin Woo Song, Tae Kon Kim, and Min-Jong Kang
- Subjects
PULMONARY fibrosis ,IDIOPATHIC pulmonary fibrosis ,REGULATORY T cells ,MYELOID cells ,GENE expression - Abstract
VISTA (V domain immunoglobulin suppressor of T cell activation, also called PD-1H [programmed death-1 homolog]), a novel immune regulator expressed on myeloid and T lymphocyte lineages, is upregulated in mouse and human idiopathic pulmonary fibrosis (IPF). However, the significance of VISTA and its therapeutic potential in regulating IPF has yet to be defined. To determine the role of VISTA and its therapeutic potential in IPF, the expression profile of VISTA was evaluated from human single-cell RNA sequencing data (IPF Cell Atlas). Inflammatory response and lung fibrosis were assessed in bleomycin-induced experimental pulmonary fibrosis models in VISTA-deficient mice compared with wild-type littermates. In addition, these outcomes were evaluated after VISTA agonistic antibody treatment in the wild-type pulmonary fibrosis mice. VISTA expression was increased in lung tissue-infiltrating monocytes of patients with IPF. VISTA was induced in the myeloid population, mainly circulating monocyte-derived macrophages, during bleomycin-induced pulmonary fibrosis. Genetic ablation of VISTA drastically promoted pulmonary fibrosis, and bleomycin-induced fibroblast activation was dependent on the interaction between VISTA-expressing myeloid cells and fibroblasts. Treatment with VISTA agonistic antibody reduced fibrotic phenotypes accompanied by the suppression of lung innate immune and fibrotic mediators. In conclusion, these results suggest that VISTA upregulation in pulmonary fibrosis may be a compensatory mechanism to limit inflammation and fibrosis, and stimulation of VISTA signaling using VISTA agonists effectively limits the fibrotic innate immune landscape and consequent tissue fibrosis. Further studies are warranted to test VISTA as a novel therapeutic target for the IPF treatment. [ABSTRACT FROM AUTHOR]
- Published
- 2023
- Full Text
- View/download PDF
5. CD38 Mediates Lung Fibrosis by Promoting Alveolar Epithelial Cell Aging.
- Author
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Huachun Cui, Na Xie, Banerjee, Sami, Dey, Tapan, Rui-Ming Liu, Antony, Veena B., Sanders, Yan Y., Adams, Taylor S., Gomez, Jose L., Thannickal, Victor J., Kaminski, Naftali, Gang Liu, Cui, Huachun, Xie, Na, Liu, Rui-Ming, and Liu, Gang
- Subjects
IDIOPATHIC pulmonary fibrosis ,LUNGS ,COENZYMES ,AGING ,RESEARCH funding ,BLEOMYCIN ,ANIMALS ,MICE ,METABOLISM - Abstract
Rationale: A prevailing paradigm recognizes idiopathic pulmonary fibrosis (IPF) originating from various alveolar epithelial cell (AEC) injuries, and there is a growing appreciation of AEC aging as a key driver of the pathogenesis. Despite this progress, it is incompletely understood what main factor(s) contribute to the worsened alveolar epithelial aging in lung fibrosis. It remains a challenge how to dampen AEC aging and thereby mitigate the disease progression. Objectives: To determine the role of AEC CD38 (cluster of differentiation 38) in promoting cellular aging and lung fibrosis. Methods: We used single-cell RNA sequencing, real-time PCR, flow cytometry, and Western blotting. Measurements and Main Results: We discovered a pivotal role of CD38, a cardinal nicotinamide adenine dinucleotide (NAD) hydrolase, in AEC aging and its promotion of lung fibrosis. We found increased CD38 expression in IPF lungs that inversely correlated with the lung functions of patients. CD38 was primarily located in the AECs of human lung parenchyma and was markedly induced in IPF AECs. Similarly, CD38 expression was elevated in the AECs of fibrotic lungs of young mice and further augmented in those of old mice, which was in accordance with a worsened AEC aging phenotype and an aggravated lung fibrosis in the old animals. Mechanistically, we found that CD38 elevation downregulated intracellular NAD, which likely led to the aging promoting impairment of the NAD-dependent cellular and molecular activities. Furthermore, we demonstrated that genetic and pharmacological inactivation of CD38 improved these NAD dependent events and ameliorated bleomycin-induced lung fibrosis. Conclusions: Our study suggests targeting alveolar CD38 as a novel and effective therapeutic strategy to treat this pathology. [ABSTRACT FROM AUTHOR]
- Published
- 2022
- Full Text
- View/download PDF
6. Single-Cell Transcriptional Archetypes of Airway Inflammation in Cystic Fibrosis
- Author
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Schupp, Jonas C., primary, Khanal, Sara, additional, Gomez, Jose L., additional, Sauler, Maor, additional, Adams, Taylor S., additional, Chupp, Geoffrey L., additional, Yan, Xiting, additional, Poli, Sergio, additional, Zhao, Yujiao, additional, Montgomery, Ruth R., additional, Rosas, Ivan O., additional, Dela Cruz, Charles S., additional, Bruscia, Emanuela M., additional, Egan, Marie E., additional, Kaminski, Naftali, additional, and Britto, Clemente J., additional
- Published
- 2020
- Full Text
- View/download PDF
7. Single Cell Analysis Reveals Novel Immune Perturbations in Fibrotic Hypersensitivity Pneumonitis.
- Author
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Zhao AY, Unterman A, Abu Hussein NS, Sharma P, Nekola F, Flint J, Yan X, Adams TS, Justet A, Sumida TS, Zhao J, Schupp JC, Raredon MSB, Ahangari F, Deluliis G, Zhang Y, Buendia-Roldan I, Adegunsoye A, Sperling AI, Prasse A, Ryu C, Herzog E, Selman M, Pardo A, and Kaminski N
- Abstract
Rationale : Fibrotic hypersensitivity pneumonitis is a debilitating interstitial lung disease driven by incompletely understood immune mechanisms. Objectives : To elucidate immune aberrations in fibrotic hypersensitivity pneumonitis in single-cell resolution. Methods : Single-cell 5' RNA sequencing was conducted on peripheral blood mononuclear cells and bronchoalveolar lavage cells obtained from 45 patients with fibrotic hypersensitivity pneumonitis, 63 idiopathic pulmonary fibrosis, 4 non-fibrotic hypersensitivity pneumonitis, and 36 healthy controls in the United States and Mexico. Analyses included differential gene expression (Seurat), transcription factor activity imputation (DoRothEA-VIPER), and trajectory analyses (Monocle3/Velocyto-scVelo-CellRank). Measurements and Main Results : Overall, 501,534 peripheral blood mononuclear cells from 110 patients and controls and 88,336 bronchoalveolar lavage cells from 19 patients were profiled. Compared to controls, fibrotic hypersensitivity pneumonitis has elevated classical monocytes (adjusted-p=2.5e-3) and are enriched in CCL3
hi /CCL4hi and S100Ahi classical monocytes (adjusted-p<2.2e-16). Trajectory analyses demonstrate that S100Ahi classical monocytes differentiate into SPP1hi lung macrophages associated with fibrosis. Compared to both controls and idiopathic pulmonary fibrosis, fibrotic hypersensitivity pneumonitis patient cells are significantly enriched in GZMhi cytotoxic T cells. These cells exhibit transcription factor activities indicative of TGFβ and TNFα/NFκB pathways. These results are publicly available at https://ildimmunecellatlas.org. Conclusions : Single-cell transcriptomics of fibrotic hypersensitivity pneumonitis patients uncovered novel immune perturbations, including previously undescribed increases in GZMhi cytotoxic CD4+ and CD8+ T cells - reflecting this disease's unique inflammatory T-cell driven nature - as well as increased S100Ahi and CCL3hi /CCL4hi classical monocytes also observed in idiopathic pulmonary fibrosis. Both cell populations may guide the development of new biomarkers and therapeutic interventions.- Published
- 2024
- Full Text
- View/download PDF
8. VISTA (PD-1H) Is a Crucial Immune Regulator to Limit Pulmonary Fibrosis.
- Author
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Kim SH, Adams TS, Hu Q, Shin HJ, Chae G, Lee SE, Sharma L, Kwon HK, Lee FY, Park HJ, Huh WJ, Manning E, Kaminski N, Sauler M, Chen L, Song JW, Kim TK, and Kang MJ
- Subjects
- Humans, Mice, Animals, Lung pathology, Fibrosis, Bleomycin pharmacology, Inflammation metabolism, Fibroblasts metabolism, Idiopathic Pulmonary Fibrosis metabolism
- Abstract
VISTA (V domain immunoglobulin suppressor of T cell activation, also called PD-1H [programmed death-1 homolog]), a novel immune regulator expressed on myeloid and T lymphocyte lineages, is upregulated in mouse and human idiopathic pulmonary fibrosis (IPF). However, the significance of VISTA and its therapeutic potential in regulating IPF has yet to be defined. To determine the role of VISTA and its therapeutic potential in IPF, the expression profile of VISTA was evaluated from human single-cell RNA sequencing data (IPF Cell Atlas). Inflammatory response and lung fibrosis were assessed in bleomycin-induced experimental pulmonary fibrosis models in VISTA-deficient mice compared with wild-type littermates. In addition, these outcomes were evaluated after VISTA agonistic antibody treatment in the wild-type pulmonary fibrosis mice. VISTA expression was increased in lung tissue-infiltrating monocytes of patients with IPF. VISTA was induced in the myeloid population, mainly circulating monocyte-derived macrophages, during bleomycin-induced pulmonary fibrosis. Genetic ablation of VISTA drastically promoted pulmonary fibrosis, and bleomycin-induced fibroblast activation was dependent on the interaction between VISTA-expressing myeloid cells and fibroblasts. Treatment with VISTA agonistic antibody reduced fibrotic phenotypes accompanied by the suppression of lung innate immune and fibrotic mediators. In conclusion, these results suggest that VISTA upregulation in pulmonary fibrosis may be a compensatory mechanism to limit inflammation and fibrosis, and stimulation of VISTA signaling using VISTA agonists effectively limits the fibrotic innate immune landscape and consequent tissue fibrosis. Further studies are warranted to test VISTA as a novel therapeutic target for the IPF treatment.
- Published
- 2023
- Full Text
- View/download PDF
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