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dc.contributor.advisorJohn E. Harris
dc.contributor.authorEssien, Kingsley I.
dc.date2022-08-11T08:08:38.000
dc.date.accessioned2022-08-23T16:01:53Z
dc.date.available2022-08-23T16:01:53Z
dc.date.issued2018-12-08
dc.date.submitted2019-04-30
dc.identifier.doi10.13028/x0vt-6m83
dc.identifier.urihttp://hdl.handle.net/20.500.14038/31233
dc.description.abstractVitiligo is an autoimmune disease of the skin characterized by epidermal depigmentation that results from CD8+ T cell-mediated destruction of pigment producing melanocytes. Vitiligo affects up to 1% of the population and current treatments are moderately effective at facilitating repigmentation by suppressing cutaneous autoimmune inflammation to promote melanocyte regeneration. In order to cause disease, CD8+ T cells must overwhelm the mechanisms of peripheral tolerance in the skin and if we understand the suppressive mechanisms that are compromised during vitiligo, we can potentially use this information to improve existing treatments or engineer novel interventions. Therefore, my goal is to characterize the regulatory factors in the skin that suppress depigmentation during vitiligo. Our lab has developed a mouse model of vitiligo that accurately reflects human disease and I used this model to demonstrate that regulatory T cells suppress CD8+ T cell-mediated depigmentation and interact with CD8+ T cells in the skin during vitiligo. In this model of disease, I investigated the molecules involved in regulatory T cell function and observed that the chemokine receptors CCR5 and CCR6 play different roles in regulatory T cell suppression. While CCR6 facilitates regulatory T cell migration to the skin, CCR5 is dispensable for migration but required for optimal regulatory T cell function. Additionally, I used our mouse model to demonstrate that Langerhans cells suppress the incidence of disease during vitiligo. Taken together the results from these studies provide novel insights into the mechanisms of suppression during vitiligo.
dc.language.isoen_US
dc.rightsCopyright is held by the author, with all rights reserved.
dc.subjectVitiligo
dc.subjectRegulatory T Cells
dc.subjectTregs
dc.subjectLangerhans cells
dc.subjectImmune System Diseases
dc.subjectImmunopathology
dc.subjectSkin and Connective Tissue Diseases
dc.titleUnderstanding regulatory factors in the skin during vitiligo
dc.typeDoctoral Dissertation
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=2024&context=gsbs_diss&unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/gsbs_diss/1015
dc.legacy.embargo2021-04-30T00:00:00-07:00
dc.identifier.contextkey14399629
refterms.dateFOA2022-08-25T05:01:15Z
html.description.abstract<p>Vitiligo is an autoimmune disease of the skin characterized by epidermal depigmentation that results from CD8+ T cell-mediated destruction of pigment producing melanocytes. Vitiligo affects up to 1% of the population and current treatments are moderately effective at facilitating repigmentation by suppressing cutaneous autoimmune inflammation to promote melanocyte regeneration. In order to cause disease, CD8+ T cells must overwhelm the mechanisms of peripheral tolerance in the skin and if we understand the suppressive mechanisms that are compromised during vitiligo, we can potentially use this information to improve existing treatments or engineer novel interventions. Therefore, my goal is to characterize the regulatory factors in the skin that suppress depigmentation during vitiligo. Our lab has developed a mouse model of vitiligo that accurately reflects human disease and I used this model to demonstrate that regulatory T cells suppress CD8+ T cell-mediated depigmentation and interact with CD8+ T cells in the skin during vitiligo. In this model of disease, I investigated the molecules involved in regulatory T cell function and observed that the chemokine receptors CCR5 and CCR6 play different roles in regulatory T cell suppression. While CCR6 facilitates regulatory T cell migration to the skin, CCR5 is dispensable for migration but required for optimal regulatory T cell function. Additionally, I used our mouse model to demonstrate that Langerhans cells suppress the incidence of disease during vitiligo. Taken together the results from these studies provide novel insights into the mechanisms of suppression during vitiligo.</p>
dc.identifier.submissionpathgsbs_diss/1015
dc.contributor.departmentDermatology
dc.description.thesisprogramInterdisciplinary Graduate Program
dc.identifier.orcid0000-0001-5299-0040


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