FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2617756735> ?p ?o ?g. }

• W2617756735 abstract "Author(s): Du, Sienmi | Advisor(s): Voskuhl, Rhonda R | Abstract: Multiple sclerosis (MS) is an autoimmune demyelinating disease characterized by increased susceptibility in women. However, when men get the disease, they demonstrate more rapid disease progression, thus presenting a clinical enigma of the pathogenic events in MS susceptibility and progression. Of the sex-related factors that may contribute to MS susceptibility, much of the literature on the MS model, experimental autoimmune encephalitomyelits (EAE), has focused on the role of sex hormones in immune responses. While sex hormones have been demonstrated to affect autoimmune responses and neurodegeneration in EAE, it does not preclude sex chromosome effects. Indeed, previous work from our lab has demonstrated that the sex chromosome complement of immune cells affected autoimmune responses, with the XX sex chromosome complement, as compared to XY, leading to greater encephalitogenicity during auto-antigen stimulation. These results are consistent with human clinical observations of increased autoimmunity in women vs. men. This dissertation builds upon this finding by exploring the nature of sex chromosome effects in the female bias in autoimmunity through the use of transgenic sex chromosome mouse models that include the following genotypes: XX, XY-, XmY*x and XpY*x. Through a series of experiments, I demonstrate that parental imprinting of the X chromosome gene, forkhead box P3 (Foxp3), a master-regulator of T regulatory (Treg) cell development, results in increased FoxP3+ Tregs in XY- mice vs. XX mice.While sex chromosome effects have been identified in the immune system, it remained unclear if there were separate sex chromosome effects in the target organ, the CNS, response to an immune attack during EAE. This question is addressed in another portion of my dissertation. I created a bone marrow chimera model with mice bearing a common immune system, but varying sex chromosome complement in the CNS using the aforementioned transgenic sex chromosome mouse models, to examine the effects of sex chromosomes in the CNS during neurodegeneration. Through a series of experiments, I demonstrated that mice with CNS cells expressing XY sex chromosome complement, as compared to XX, led to greater neurodegeneration. Further, increased neurodegenerative response in the XY CNS was due to the maternal X allele. Together, these results demonstrated for the first time an affect of parental imprinting resulting in female bias on the autoimmune responses, and male bias in neurodegeneration during EAE. These findings may bear relevance to the clinical observations of female bias in susceptibility, but increased disability progression in men with MS." @default.
• W2617756735 created "2017-06-05" @default.
• W2617756735 creator A5016336671 @default.
• W2617756735 date "2015-01-01" @default.
• W2617756735 modified "2023-09-27" @default.
• W2617756735 title "Parent-of-Origin Sex Chromosome Effects on the Immune and Central Nervous System During Experimental Autoimmune Encephalomyelitis" @default.
• W2617756735 hasPublicationYear "2015" @default.
• W2617756735 type Work @default.
• W2617756735 sameAs 2617756735 @default.
• W2617756735 citedByCount "0" @default.
• W2617756735 crossrefType "journal-article" @default.
• W2617756735 hasAuthorship W2617756735A5016336671 @default.
• W2617756735 hasConcept C104317684 @default.
• W2617756735 hasConcept C159654299 @default.
• W2617756735 hasConcept C203014093 @default.
• W2617756735 hasConcept C2778486448 @default.
• W2617756735 hasConcept C2779075594 @default.
• W2617756735 hasConcept C2779727006 @default.
• W2617756735 hasConcept C2780130043 @default.
• W2617756735 hasConcept C2780640218 @default.
• W2617756735 hasConcept C35158069 @default.
• W2617756735 hasConcept C54355233 @default.
• W2617756735 hasConcept C86803240 @default.
• W2617756735 hasConcept C8891405 @default.
• W2617756735 hasConceptScore W2617756735C104317684 @default.
• W2617756735 hasConceptScore W2617756735C159654299 @default.
• W2617756735 hasConceptScore W2617756735C203014093 @default.
• W2617756735 hasConceptScore W2617756735C2778486448 @default.
• W2617756735 hasConceptScore W2617756735C2779075594 @default.
• W2617756735 hasConceptScore W2617756735C2779727006 @default.
• W2617756735 hasConceptScore W2617756735C2780130043 @default.
• W2617756735 hasConceptScore W2617756735C2780640218 @default.
• W2617756735 hasConceptScore W2617756735C35158069 @default.
• W2617756735 hasConceptScore W2617756735C54355233 @default.
• W2617756735 hasConceptScore W2617756735C86803240 @default.
• W2617756735 hasConceptScore W2617756735C8891405 @default.
• W2617756735 hasLocation W26177567351 @default.
• W2617756735 hasOpenAccess W2617756735 @default.
• W2617756735 hasPrimaryLocation W26177567351 @default.
• W2617756735 hasRelatedWork W1521040928 @default.
• W2617756735 hasRelatedWork W1594362885 @default.
• W2617756735 hasRelatedWork W1988353904 @default.
• W2617756735 hasRelatedWork W2024277710 @default.
• W2617756735 hasRelatedWork W2034815827 @default.
• W2617756735 hasRelatedWork W2045393977 @default.
• W2617756735 hasRelatedWork W2048403952 @default.
• W2617756735 hasRelatedWork W2159287338 @default.
• W2617756735 hasRelatedWork W2160569592 @default.
• W2617756735 hasRelatedWork W2401414316 @default.
• W2617756735 hasRelatedWork W2612805522 @default.
• W2617756735 hasRelatedWork W27615877 @default.
• W2617756735 hasRelatedWork W2884662215 @default.
• W2617756735 hasRelatedWork W2887419763 @default.
• W2617756735 hasRelatedWork W2968552237 @default.
• W2617756735 hasRelatedWork W3099658284 @default.
• W2617756735 hasRelatedWork W3120156106 @default.
• W2617756735 hasRelatedWork W3135046858 @default.
• W2617756735 hasRelatedWork W3100904600 @default.
• W2617756735 isParatext "false" @default.
• W2617756735 isRetracted "false" @default.
• W2617756735 magId "2617756735" @default.
• W2617756735 workType "article" @default.