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Your search keyword '"Harris, John E."' showing total 23 results
Start Over Author "Harris, John E." Journal journal of investigative dermatology
23 results on '"Harris, John E."'

1. CXCL9 Links Skin Inflammation and Fibrosis through CXCR3-Dependent Upregulation of Col1a1 in Fibroblasts

Author

Richmond, Jillian M., Patel, Dhrumil, Watanabe, Tomoya, Chen, Henry W., Martyanov, Viktor, Werner, Giffin, Garg, Madhuri, Haddadi, Nazgol-Sadat, Refat, Maggi Ahmed, Mahmoud, Bassel H., Wong, Lance D., Dresser, Karen, Deng, April, Zhu, Jane L., McAlpine, William, Hosler, Gregory A., Feghali-Bostwick, Carol A., Whitfield, Michael L., Harris, John E., Torok, Kathryn S., and Jacobe, Heidi T.

Published
2023
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11. CXCL9 links skin inflammation and fibrosis via CXCR3-dependent upregulation of collagen 1a1 in fibroblasts

Author

Richmond, Jillian M., primary, Patel, Dhrumil, additional, Watanabe, Tomoya, additional, Chen, Henry W., additional, Martyanov, Viktor, additional, Werner, Giffin, additional, Garg, Madhuri, additional, Haddadi, Nazgol-Sadat, additional, Refat, Maggi Ahmed, additional, Mahmoud, Bassel H., additional, Wong, Lance D., additional, Dresser, Karen, additional, Deng, April, additional, Zhu, Jane L., additional, McAlpine, William, additional, Hosler, Gregory A., additional, Feghali-Bostwick, Carol A., additional, Whitfield, Michael L., additional, Harris, John E., additional, Torok, Kathryn S., additional, and Jacobe, Heidi T., additional

Published
2023
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18. Neutrophils Self-Regulate Immune Complex-Mediated Cutaneous Inflammation through CXCL2

Author

Li, Jackson LiangYao, primary, Lim, Chun Hwee, additional, Tay, Fen Wei, additional, Goh, Chi Ching, additional, Devi, Sapna, additional, Malleret, Benoit, additional, Lee, Bernett, additional, Bakocevic, Nadja, additional, Chong, Shu Zhen, additional, Evrard, Maximilien, additional, Tanizaki, Hideaki, additional, Lim, Hwee Ying, additional, Russell, Bruce, additional, Renia, Laurent, additional, Zolezzi, Francesca, additional, Poidinger, Michael, additional, Angeli, Veronique, additional, St. John, Ashley L., additional, Harris, John E., additional, Tey, Hong Liang, additional, Tan, Suet Mien, additional, Kabashima, Kenji, additional, Weninger, Wolfgang, additional, Larbi, Anis, additional, and Ng, Lai Guan, additional

Published
2016
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20. CXCL9 Links Skin Inflammation and Fibrosis through CXCR3-Dependent Upregulation of Col1a1in Fibroblasts

Author

Richmond, Jillian M., Patel, Dhrumil, Watanabe, Tomoya, Chen, Henry W., Martyanov, Viktor, Werner, Giffin, Garg, Madhuri, Haddadi, Nazgol-Sadat, Refat, Maggi Ahmed, Mahmoud, Bassel H., Wong, Lance D., Dresser, Karen, Deng, April, Zhu, Jane L., McAlpine, William, Hosler, Gregory A., Feghali-Bostwick, Carol A., Whitfield, Michael L., Harris, John E., Torok, Kathryn S., and Jacobe, Heidi T.

Abstract

Morphea is characterized by initial inflammation followed by fibrosis of the skin and soft tissue. Despite its substantial morbidity, the pathogenesis of morphea is poorly studied. Previous work showed that CXCR3 ligands CXCL9 and CXCL10 are highly upregulated in the sera and lesional skin of patients with morphea. We found that an early inflammatory subcutaneous bleomycin mouse model of dermal fibrosis mirrors the clinical, histological, and immune dysregulation observed in human morphea. We used this model to examine the role of the CXCR3 chemokine axis in the pathogenesis of cutaneous fibrosis. Using the REX3 (Reporting the Expression of CXCR3 ligands) mice, we characterized which cells produce CXCR3 ligands over time. We found that fibroblasts contribute the bulk of CXCL9-RFP and CXCL10-BFP by percentage, whereas macrophages produce high amounts on a per-cell basis. To determine whether these chemokines are mechanistically involved in pathogenesis, we treated Cxcl9-, Cxcl10-, or Cxcr3-deficient mice with bleomycin and found that fibrosis is dependent on CXCL9 and CXCR3. Addition of recombinant CXCL9 but not CXCL10 to cultured mouse fibroblasts induced Col1a1mRNA expression, indicating that the chemokine itself contributes to fibrosis. Taken together, our studies provide evidence that CXCL9 and its receptor CXCR3 are functionally required for inflammatory fibrosis.

Published
2023
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23. A Mouse Model of Vitiligo with Focused Epidermal Depigmentation Requires IFN-γ for Autoreactive CD8+ T-Cell Accumulation in the Skin.

Author

Harris, John E, Harris, Tajie H, Weninger, Wolfgang, Wherry, E John, Hunter, Christopher A, and Turka, Laurence A

Subjects
*VITILIGO, *LABORATORY mice, *EPIDERMAL diseases, *CD80 antigen, *T cells, *BIOACCUMULATION, *INTERFERONS, *MELANOCYTES
Abstract

Vitiligo is an autoimmune disease of the skin causing disfiguring patchy depigmentation of the epidermis and, less commonly, hair. Therapeutic options for vitiligo are limited, reflecting in part limited knowledge of disease pathogenesis. Existing mouse models of vitiligo consist of hair depigmentation but lack prominent epidermal involvement, which is the hallmark of human disease. They are thus unable to provide a platform to fully investigate disease mechanisms and treatment. CD8+ T cells have been implicated in the pathogenesis of vitiligo, and expression of IFN-γ is increased in the lesional skin of patients, however, it is currently unknown what role IFN-γ has in disease. Here, we have developed an adoptive transfer mouse model of vitiligo using melanocyte-specific CD8+ T cells, which recapitulates the human condition by inducing epidermal depigmentation while sparing the hair. Like active lesions in human vitiligo, histology of depigmenting skin reveals a patchy mononuclear infiltrate and single-cell infiltration of the epidermis. Depigmentation is accompanied by accumulation of autoreactive CD8+ T cells in the skin, quantifiable loss of tyrosinase transcript, and local IFN-γ production. Neutralization of IFN-γ with antibody prevents CD8+ T-cell accumulation and depigmentation, suggesting a therapeutic potential for this approach. [ABSTRACT FROM AUTHOR]

Published
2012
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