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Your search keyword '"Wolf, Sonya"' showing total 22 results
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22 results on '"Wolf, Sonya"'

1. Macrophage-specific inhibition of the histone demethylase JMJD3 decreases STING and pathologic inflammation in diabetic wound repair

Author

Audu, Christopher O., Melvin, William J., Joshi, Amrita D., Wolf, Sonya J., Moon, Jadie Y., Davis, Frank M., Barrett, Emily C., Mangum, Kevin D., Deng, Hongping, Xing, Xianying, Wasikowski, Rachel, Tsoi, Lam C., Sharma, Sriganesh B., Bauer, Tyler M., Shadiow, James, Corriere, Matthew A., Obi, Andrea T., Kunkel, Steven L., Levi, Benjamin, Moore, Bethany B., Gudjonsson, Johann E., Smith, Andrew M., and Gallagher, Katherine A.

Published
2022
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2. Coronavirus induces diabetic macrophage-mediated inflammation via SETDB2

Author

Melvin, William J., Audu, Christopher O., Davis, Frank M., Sharma, Sriganesh B., Joshi, Amrita, DenDekker, Aaron, Wolf, Sonya, Barrett, Emily, Mangum, Kevin, Zhou, Xiaofeng, Bame, Monica, Ruan, Alex, Obi, Andrea, Kunkel, Steven L., Moore, Bethany B., and Gallagher, Katherine A.

Published
2021

10. IFN-κ is critical for normal wound repair and is decreased in diabetic wounds

Author

Wolf, Sonya J., primary, Audu, Christopher O., additional, Joshi, Amrita, additional, denDekker, Aaron, additional, Melvin, William J., additional, Davis, Frank M., additional, Xing, Xianying, additional, Wasikowski, Rachael, additional, Tsoi, Lam C., additional, Kunkel, Steven L., additional, Gudjonsson, Johann E., additional, O’Riordan, Mary X., additional, Kahlenberg, J. Michelle, additional, and Gallagher, Katherine A., additional

Published
2022
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14. Inhibition of macrophage histone demethylase JMJD3 protects against abdominal aortic aneurysms

Author

Davis, Frank M., primary, Tsoi, Lam C., additional, Melvin, William J., additional, denDekker, Aaron, additional, Wasikowski, Rachael, additional, Joshi, Amrita D., additional, Wolf, Sonya, additional, Obi, Andrea T., additional, Billi, Allison C., additional, Xing, Xianying, additional, Audu, Christopher, additional, Moore, Bethany B., additional, Kunkel, Steven L., additional, Daugherty, Alan, additional, Lu, Hong S., additional, Gudjonsson, Johann E., additional, and Gallagher, Katherine A., additional

Published
2021
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15. Epigenetic regulation of the PGE2 pathway modulates macrophage phenotype in normal and pathologic wound repair

Author

Davis, Frank M., primary, Tsoi, Lam C., additional, Wasikowski, Rachael, additional, denDekker, Aaron, additional, Joshi, Amrita, additional, Wilke, Carol, additional, Deng, Hongping, additional, Wolf, Sonya, additional, Obi, Andrea, additional, Huang, Steven, additional, Billi, Allison C., additional, Robinson, Scott, additional, Lipinski, Jay, additional, Melvin, William J., additional, Audu, Christopher O., additional, Weidinger, Stephan, additional, Kunkel, Steven L., additional, Smith, Andrew, additional, Gudjonsson, Johann E., additional, Moore, Bethany B., additional, and Gallagher, Katherine A., additional

Published
2020
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17. TNF-α regulates diabetic macrophage function through the histone acetyltransferase MOF

Author

denDekker, Aaron D., primary, Davis, Frank M., additional, Joshi, Amrita D., additional, Wolf, Sonya J., additional, Allen, Ronald, additional, Lipinski, Jay, additional, Nguyen, Brenda, additional, Kirma, Joseph, additional, Nycz, Dylan, additional, Bermick, Jennifer, additional, Moore, Bethany B., additional, Gudjonsson, Johann E., additional, Kunkel, Steven L., additional, and Gallagher, Katherine A., additional

Published
2020
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18. The female-biased factor VGLL3 drives cutaneous and systemic autoimmunity

Author

Billi, Allison C., primary, Gharaee-Kermani, Mehrnaz, additional, Fullmer, Joseph, additional, Tsoi, Lam C., additional, Hill, Brett D., additional, Gruszka, Dennis, additional, Ludwig, Jessica, additional, Xing, Xianying, additional, Estadt, Shannon, additional, Wolf, Sonya J., additional, Rizvi, Syed Monem, additional, Berthier, Celine C., additional, Hodgin, Jeffrey B., additional, Beamer, Maria A., additional, Sarkar, Mrinal K., additional, Liang, Yun, additional, Uppala, Ranjitha, additional, Shao, Shuai, additional, Zeng, Chang, additional, Harms, Paul W., additional, Verhaegen, Monique E., additional, Voorhees, John J., additional, Wen, Fei, additional, Ward, Nicole L., additional, Dlugosz, Andrzej A., additional, Kahlenberg, J. Michelle, additional, and Gudjonsson, Johann E., additional

Published
2019
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20. IFN-κ Is a Rheostat for Development of Psoriasiform Inflammation

Author

Gharaee-Kermani, Mehrnaz, Estadt, Shannon N., Tsoi, Lam C., Wolf, Sonya J., Liu, Jianhua, Xing, Xianying, Theros, Jonathon, Reed, Tammi J., Lowe, Lori, Gruszka, Dennis, Ward, Nicole L., Gudjonsson, Johann E., and Kahlenberg, J. Michelle

Abstract

Psoriasis is a common, inflammatory autoimmune skin disease. Early detection of an IFN-1 signature occurs in many psoriasis lesions, but the source of IFN production remains debated. IFN-κ is an important source of IFN-1 production in the epidermis. We identified a correlation between IFN-regulated and psoriasis-associated genes in human lesional skin. We thus wanted to explore the effects of IFN-κ in psoriasis using the well-characterized imiquimod psoriasis model. Three mouse strains aged 10 weeks were used: wild-type C57Bl/6, C57Bl/6 that overexpress Ifnkin the epidermis (i.e., transgenic), and total body Ifnk–/–(i.e., knockout) strain. Psoriasis was induced by topical application of imiquimod on both ears for 8 consecutive days. Notably, the severity of skin lesions and inflammatory cell infiltration was more significantly increased in transgenic than in wild-type than in knockout mice. Gene expression analysis identified a more upregulation of Mxa, Il1b, Tnfa, Il6, Il12, Il23, Il17,and Ifngin transgenic than in wild-type than in knockout mice after imiquimod treatment. Furthermore, imiquimod increased CD8+and CD4+T-cell infiltration more in transgenic than in wild-type than in knockout mice. In summary, we identified IFN-κ as a rheostat for initiation of psoriasiform inflammation. This suggests that targeting IFN-1s early in the disease may be an effective way of controlling psoriatic inflammation.

Published
2021
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21. The histone methyltransferase mixed-lineage-leukemia-1 drives T cell phenotype via notch signaling in diabetic tissue repair.

Author

Melvin WJ, Bauer TM, Magnum KD, Audu CO, Shadiow J, Barrett E, Joshi A, Moon JY, Bogel R, Mazumder P, Wolf SJ, Kunkel S, Gudjonsson JE, Davis FM, and Gallagher KA

Abstract

Immune cell mediated inflammation is important in normal tissue regeneration but can be pathologic in diabetic wounds. Limited literature exists on the role of CD4+T cells in normal or diabetic wound repair, however, the imbalance of CD4+TH17/Treg cells has been found to promote inflammation in other diabetic tissues. Here, using human tissue and murine transgenic models, we identified that the histone methyltransferase MLL1 directly regulates the TH17 transcription factor RORγ via an H3K4me3 mechanism and increases expression of Notch receptors and downstream Notch signaling. Further, we found that Notch receptor signaling regulates CD4+TH cell differentiation and is critical for normal wound repair, and loss of upstream Notch pathway mediators or receptors in CD4+T cells resulted in the loss of CD4+TH cell differentiation in wounds. In diabetes, MLL1 and Notch-receptor signaling were upregulated in wound CD4+TH cells, driving CD4+ T cells towards the TH17 cell phenotype. Treatment of diabetic wound CD4T cells with a small molecule inhibitor of MLL1 (MI-2) yielded a significant reduction in CD4+TH17 cells and IL17A. This is the first study to identify the MLL1-mediated mechanisms responsible for regulating the TH17/Treg balance in normal and diabetic wounds and define the complex role of Notch signaling in CD4+T cells in wounds, where increased or decreased Notch signaling both result in pathologic wound repair. Therapeutic targeting of MLL1 in diabetic CD4+TH cells may decrease pathologic inflammation through regulation of CD4+T cell differentiation.

Published
2024
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22. Histone demethylase JARID1C/KDM5C regulates Th17 cells by increasing IL-6 expression in diabetic plasmacytoid dendritic cells.

Author

Audu CO, Wolf SJ, Joshi AD, Moon JY, Melvin WJ, Sharma SB, Davis FM, Obi AT, Wasikowski R, Tsoi LC, Barrett EC, Mangum KD, Bauer TM, Kunkel SL, Moore BB, and Gallagher KA

Subjects
Animals, Female, Humans, Male, Mice, Interleukin-17 metabolism, Jumonji Domain-Containing Histone Demethylases metabolism, Jumonji Domain-Containing Histone Demethylases genetics, Mice, Inbred C57BL, Dendritic Cells immunology, Dendritic Cells metabolism, Interleukin-6 metabolism, Th17 Cells immunology, Th17 Cells metabolism, Wound Healing immunology
Abstract

Plasmacytoid dendritic cells (pDCs) are first responders to tissue injury, where they prime naive T cells. The role of pDCs in physiologic wound repair has been examined, but little is known about pDCs in diabetic wound tissue and their interactions with naive CD4+ T cells. Diabetic wounds are characterized by increased levels of inflammatory IL-17A cytokine, partly due to increased Th17 CD4+ cells. This increased IL-17A cytokine, in excess, impairs tissue repair. Here, using human tissue and murine wound healing models, we found that diabetic wound pDCs produced excess IL-6 and TGF-β and that these cytokines skewed naive CD4+ T cells toward a Th17 inflammatory phenotype following cutaneous injury. Further, we identified that increased IL-6 cytokine production by diabetic wound pDCs is regulated by a histone demethylase, Jumonji AT-rich interactive domain 1C histone demethylase (JARID1C). Decreased JARID1C increased IL-6 transcription in diabetic pDCs, and this process was regulated upstream by an IFN-I/TYK2/JAK1,3 signaling pathway. When inhibited in nondiabetic wound pDCs, JARID1C skewed naive CD4+ T cells toward a Th17 phenotype and increased IL-17A production. Together, this suggests that diabetic wound pDCs are epigenetically altered to increase IL-6 expression that then affects T cell phenotype. These findings identify a therapeutically manipulable pathway in diabetic wounds.

Published
2024
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