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25 results on '"Wang, Wei-Le"'

5. A Cre-deleter specific for embryo-derived brain macrophages reveals distinct features of microglia and border macrophages

Author

Brioschi, Simone, primary, Belk, Julia A., additional, Peng, Vincent, additional, Molgora, Martina, additional, Rodrigues, Patrick Fernandes, additional, Nguyen, Khai M., additional, Wang, Shoutang, additional, Du, Siling, additional, Wang, Wei-Le, additional, Grajales-Reyes, Gary E., additional, Ponce, Jennifer M., additional, Yuede, Carla M., additional, Li, Qingyun, additional, Baer, John M., additional, DeNardo, David G., additional, Gilfillan, Susan, additional, Cella, Marina, additional, Satpathy, Ansuman T., additional, and Colonna, Marco, additional

Published
2023
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7. The aryl hydrocarbon receptor instructs the immunomodulatory profile of a subset of Clec4a4 + eosinophils unique to the small intestine

Author

Wang, Wei-Le, primary, Kasamatsu, Jun, additional, Joshita, Satoru, additional, Gilfillan, Susan, additional, Di Luccia, Blanda, additional, Panda, Santosh K., additional, Kim, Do-Hyun, additional, Desai, Pritesh, additional, Bando, Jennifer K., additional, Huang, Stanley Ching-Cheng, additional, Yomogida, Kentaro, additional, Hoshino, Hitomi, additional, Fukushima, Mana, additional, Jacobsen, Elizabeth A., additional, Van Dyken, Steven J., additional, Ruedl, Christiane, additional, Cella, Marina, additional, and Colonna, Marco, additional

Published
2022
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11. Heterogeneity of meningeal B cells reveals a lymphopoietic niche at the CNS borders

Author

Brioschi, Simone, primary, Wang, Wei-Le, additional, Peng, Vincent, additional, Wang, Meng, additional, Shchukina, Irina, additional, Greenberg, Zev J., additional, Bando, Jennifer K., additional, Jaeger, Natalia, additional, Czepielewski, Rafael S., additional, Swain, Amanda, additional, Mogilenko, Denis A., additional, Beatty, Wandy L., additional, Bayguinov, Peter, additional, Fitzpatrick, James A. J., additional, Schuettpelz, Laura G., additional, Fronick, Catrina C., additional, Smirnov, Igor, additional, Kipnis, Jonathan, additional, Shapiro, Virginia S., additional, Wu, Gregory F., additional, Gilfillan, Susan, additional, Cella, Marina, additional, Artyomov, Maxim N., additional, Kleinstein, Steven H., additional, and Colonna, Marco, additional

Published
2021
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12. microRNA-142 guards against autoimmunity by controlling Treg cell homeostasis and function.

Author

Wang, Wei-Le, Ouyang, Ching, Graham, Natalie M., Zhang, Yuankun, Cassady, Kaniel, Reyes, Estefany Y., Xiong, Min, Davis, Alicia M., Tang, Kathie, Zeng, Defu, and Boldin, Mark P.

Subjects
*CELL physiology, *REGULATORY T cells, *AUTOIMMUNITY, *INTERFERON gamma, *IMMUNOLOGICAL tolerance, *T helper cells
Abstract

Regulatory T (Treg) cells are critical in preventing aberrant immune responses. Posttranscriptional control of gene expression by microRNA (miRNA) has recently emerged as an essential genetic element for Treg cell function. Here, we report that mice with Treg cell–specific ablation of miR-142 (hereafter Foxp3CremiR-142fl/fl mice) developed a fatal systemic autoimmune disorder due to a breakdown in peripheral T-cell tolerance. Foxp3CremiR-142fl/fl mice displayed a significant decrease in the abundance and suppressive capacity of Treg cells. Expression profiling of miR-142–deficient Treg cells revealed an up-regulation of multiple genes in the interferon gamma (IFNγ) signaling network. We identified several of these IFNγ-associated genes as direct miR-142-3p targets and observed excessive IFNγ production and signaling in miR-142–deficient Treg cells. Ifng ablation rescued the Treg cell homeostatic defect and alleviated development of autoimmunity in Foxp3CremiR-142fl/fl mice. Thus, our findings implicate miR-142 as an indispensable regulator of Treg cell homeostasis that exerts its function by attenuating IFNγ responses. This study identifies microRNA-142 as a central regulator of the development, homeostasis and function of regulatory T cells. Mechanistically, the miR-142-3p isoform controls regulatory T cell homeostasis and immune tolerance by attenuating IFNγ responses. [ABSTRACT FROM AUTHOR]

Published
2022
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14. MicroRNA-142 Is Critical for the Homeostasis and Function of Type 1 Innate Lymphoid Cells

Author

Berrien-Elliott, Melissa M., primary, Sun, Yaping, additional, Neal, Carly, additional, Ireland, Aaron, additional, Trissal, Maria C., additional, Sullivan, Ryan P., additional, Wagner, Julia A., additional, Leong, Jeffrey W., additional, Wong, Pamela, additional, Mah-Som, Annelise Y., additional, Wong, Terrence N., additional, Schappe, Timothy, additional, Keppel, Catherine R., additional, Cortez, Victor S., additional, Stamatiades, Efstathios G., additional, Li, Ming O., additional, Colonna, Marco, additional, Link, Daniel C., additional, French, Anthony R., additional, Cooper, Megan A., additional, Wang, Wei-Le, additional, Boldin, Mark P., additional, Reddy, Pavan, additional, and Fehniger, Todd A., additional

Published
2019
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16. Downregulation of Mir-142 Promotes Leukemia Growth in Philadelphia Chromosome-Positive (Ph+) Acute Lymphoblastic Leukemia (ALL): A Possible Novel Therapeutic Target?

Author

Wang, Huafeng, primary, Zhang, Bin, additional, Wang, Wei-Le, additional, Zhao, Dandan, additional, Li, Ling, additional, Wu, Herman, additional, Nguyen, Le Xuan Truong, additional, Meng, Weixu, additional, McDonald, Tinisha, additional, Pichiorri, Flavia, additional, Kuo, Ya-Huei, additional, Chen, Jianjun, additional, Carlesso, Nadia, additional, Aldoss, Ibrahim, additional, Pullarkat, Vinod A., additional, Al Malki, Monzr, additional, Stein, Anthony S., additional, Boldin, Mark, additional, Jin, Jie, additional, and Marcucci, Guido, additional

Published
2018
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19. Acquired microRNA-142 Deficit Drives Escape Mechanisms of Anti-Leukemic Surveillance during Blast Crisis Transformation of Chronic Myeloid Leukemia (CML)

Author

Chen, Fang, Zhao, Dandan, Zhang, Yi, Xu, Yongfang, Chen, Min-Hsuan, Pathak, Khyatiben V., Liang, Yong, Wang, Wei-Le, Estrella, Katrina, Wu, Xiwei, Ghoda, Lucy Y., Kuo, Ya-Huei, Ali, Haris, Yu, Jianhua, Caligiuri, Michael A, Boldin, Mark, Swiderski, Piotr, Kortylewski, Marcin, Pirrotte, Patrick, Nguyen, Le Xuan Truong, Marcucci, Guido, and Zhang, Bin

Abstract

CML may evolve from a chronic phase (CP) into blast crisis (BC), but the underlying mechanisms of the transformation remain to be fully elucidated. We reported that microRNA (miR)-142 is downregulated in BC compared with CP patients; and in a murine model of CP CML (i.e., BCR-ABLmouse), miR-142 knock-out (KO) induced a BC-like phenotype, substantiating a mechanistic role of miR-142 deficit in BC transformation. Mechanistically, miR-142 KO induced mitochondrial fusion and increased oxidative phosphorylation (OxPhos) in leukemic stem cells (LSCs), causing a shift of leukemic phenotype from CP to BC ( Nat Commun, in press). Herein, we report that miR-142 deficit also occurs in T lymphocytes of BC patients due to inflammatory cytokines that are aberrantly produced by the proliferating leukemic cells. Using the Mir142 −/−BCR-ABLmouse, we observed that miR-142 deficit resulted in loss of T cell number and activity, suppressed the antileukemic immune surveillance, and contributed to BC transformation. In fact, miR-142 KO hampered thymic lymphoid-primed multipotent progenitor (LMPP) differentiation into T cells and rendered mature T cells dysfunctional and exhausted, with increase of PD-1 levels, and decrease of the apoptotic threshold, cell cycling and cytokine production, via blockade of OxPhos/glycolysis switch that regulates the metabolism of otherwise activated T cells. These changes translated into a decrease of T-cell antileukemic surveillance as demonstrated by increased numbers of BC murine Lin -Sca-1 +c-Kit +(LSKs) or human CD34+ blasts cocultured with Mir142 −/−T-cells vs those cocultured with Mir142 +/+T-cells. Furthermore, congenic B6 (lethally irradiated to eradicate host T cells) or immunodeficient NSG (no T cells) recipient mice transplanted with Mir142 −/−BCR-ABLLSK and Mir142 −/−T cells had reduced T cells (both: p<0.0001), increased blasts (B6: p=0.01; NSG: p<0.0001) and a shorter survival (median survival for B6: 58 days vs unreached, p=0.008; for NSG: 28 days vs unreached, p<0.0001) compared with the respective controls transplanted with Mir142 −/−BCR-ABLLSK and Mir142 +/+T cells. Transplantation of Mir142 −/−BCR-ABLLSKs into Mir142 −/−or Mir142 flox(f)/fLck-cre+(i.e., miR-142 KO only in T cells; Mir142T Δ/Δ) recipients also resulted in a shorter survival than Mir142 +/+recipients (median survival for Mir142 −/−vs Mir142 +/+recipients: 44 vs 53 days, p=0.001; for Mir142T Δ/Δvs Mir142 +/+recipients: 42 vs 53 days, p=0.0002).

Published
2023
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22. R26R-GR: A Cre-Activable Dual Fluorescent Protein Reporter Mouse

Author

Chen, You-Tzung, primary, Tsai, Ming-Shian, additional, Yang, Tsung-Lin, additional, Ku, Amy Tsu, additional, Huang, Ke-Han, additional, Huang, Cheng-Yen, additional, Chou, Fu-Ju, additional, Fan, Hsiang-Hsuan, additional, Hong, Jin-Bon, additional, Yen, Shuo-Ting, additional, Wang, Wei-Le, additional, Lin, Chang-Ching, additional, Hsu, Yu-Chen, additional, Su, Kang-Yi, additional, Su, I-Chang, additional, Jang, Chuan-Wei, additional, Behringer, Richard R., additional, Favaro, Rebecca, additional, Nicolis, Silvia K., additional, Chien, Chung-Liang, additional, Lin, Shu-Wha, additional, and Yu, I-Shing, additional

Published
2012
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23. Design of a Monitoring and Controlling System for Poultry Breeding.

Author

Wang Wei-le, Gao Jun-li, Zhu Hui-hua, and Chen Wei

Abstract

According to automatic poultry breeding, this paper discusses a design for automatic monitoring system of poultry breeding. This system takes each breeding house a single unit. By taking the advantage of ADAM model, environmental detection model and PC Auto configuration software, the environmental parameters of the breeding houses, including temperature, humidity, illumination intensity and harmful gas concentration are automatically monitored. Indoor lights, curtains, spray equipment can also be automatically controlled. The test proves the design stable performance and great practicality. [ABSTRACT FROM AUTHOR]

Published
2015
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24. Altered lymphopoiesis and immunodeficiency in miR-142null mice

Author

Kramer, Nicholas J., Wang, Wei-Le, Reyes, Estefany Y., Kumar, Bijender, Chen, Ching-Cheng, Ramakrishna, Chandran, Cantin, Edouard M., Vonderfecht, Steven L., Taganov, Konstantin D., Chau, Nelson, and Boldin, Mark P.

Abstract

MicroRNAs (miRNAs) are a class of powerful posttranscriptional regulators implicated in the control of diverse biological processes, including regulation of hematopoiesis and the immune response. To define the biological functions of miR-142, which is preferentially and abundantly expressed in immune cells, we created a mouse line with a targeted deletion of this gene. Our analysis of miR-142−/−mice revealed a critical role for this miRNA in the development and homeostasis of lymphocytes. Marginal zone B cells expand in the knockout spleen, whereas the number of T and B1 B cells in the periphery is reduced. Abnormal development of hematopoietic lineages in miR-142−/−animals is accompanied by a profound immunodeficiency, manifested by hypoimmunoglobulinemia and failure to mount a productive immune response to soluble antigens and virus. miR-142−/−B cells express elevated levels of B-cell–activating factor (BAFF) receptor (BAFF-R) and as a result proliferate more robustly in response to BAFF stimulation. Lowering the BAFF-Rgene dose in miR-142−/−mice rescues the B-cell expansion defect, suggesting that BAFF-Ris a bona fide miR-142target through which it controls B-cell homeostasis. Collectively, our results uncover miR-142as an essential regulator of lymphopoiesis, and suggest that lesions in this miRNA gene may lead to primary immunodeficiency.

Published
2015
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25. The epithelial C15ORF48/miR-147-NDUFA4 axis is an essential regulator of gut inflammation, energy metabolism, and the microbiome.

Author

Xiong M, Liu Z, Wang B, Sokolich T, Graham N, Chen M, Wang WL, and Boldin MP

Subjects
Animals, Humans, Mice, Colitis metabolism, Colitis microbiology, Colitis genetics, Colitis chemically induced, Dysbiosis metabolism, Dysbiosis microbiology, Inflammatory Bowel Diseases metabolism, Inflammatory Bowel Diseases microbiology, Inflammatory Bowel Diseases genetics, Intestinal Mucosa metabolism, Intestinal Mucosa microbiology, Mice, Inbred C57BL, NF-kappa B metabolism, Signal Transduction, Energy Metabolism genetics, Gastrointestinal Microbiome, Inflammation metabolism, MicroRNAs genetics, MicroRNAs metabolism
Abstract

Chronic inflammation is epidemiologically linked to the pathogenesis of gastrointestinal diseases, including inflammatory bowel disease (IBD) and colorectal cancer (CRC). However, our understanding of the molecular mechanisms controlling gut inflammation remains insufficient, hindering the development of targeted therapies for IBD and CRC. In this study, we uncovered C15ORF48/miR-147 as a negative regulator of gut inflammation, operating through the modulation of epithelial cell metabolism. C15ORF48/miR-147 encodes two molecular products, C15ORF48 protein and miR-147-3p microRNA, which are predominantly expressed in the intestinal epithelium. C15ORF48/miR-147 ablation leads to gut dysbiosis and exacerbates chemically induced colitis in mice. C15ORF48 and miR-147-3p work together to suppress colonocyte metabolism and inflammation by silencing NDUFA4 , a subunit of mitochondrial complex IV (CIV). Interestingly, the C15ORF48 protein, a structural paralog of NDUFA4, contains a unique C-terminal α-helical domain crucial for displacing NDUFA4 from CIV and its subsequent degradation. NDUFA4 silencing hinders NF-κB signaling activation and consequently attenuates inflammatory responses. Collectively, our findings have established the C15ORF48/miR-147 - NDUFA4 molecular axis as an indispensable regulator of gut homeostasis, bridging mitochondrial metabolism and inflammation., Competing Interests: Competing interests statement:The authors declare no competing interest.

Published
2024
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