자료유형  

 학위논문

Control Number  

0016934597

International Standard Book Number  

9798380594844

Dewey Decimal Classification Number  

616.079

Main Entry-Personal Name  

Thompson, Jacob William.

Publication, Distribution, etc. (Imprint  

[S.l.] : The University of Utah., 2023

Publication, Distribution, etc. (Imprint  

Ann Arbor : ProQuest Dissertations & Theses, 2023

Physical Description  

1 online resource(67 p.)

General Note  

Source: Dissertations Abstracts International, Volume: 85-04, Section: B.

General Note  

Advisor: O'Connell, Ryan M.

Dissertation Note  

Thesis (Ph.D.)--The University of Utah, 2023.

Restrictions on Access Note  

This item must not be sold to any third party vendors.

Summary, Etc.  

요약During neuroinflammation, immune cells infiltrating into the CNS express and release a wide range of factors to either drive inflammation or keep it under control. This balance is regulated in part by a pro-inflammatory microRNA-155. miR-155 is expressed highly in the serum and CNS lesions of patients with multiple sclerosis. Mice lacking miR-155 have reduced disease severity during the progression of experimental autoimmune encephalomyelitis (EAE), due in part to a reduction in CNS-infiltrating Th17 T cells. I was able to utilize single-cell RNA sequencing to clearly demonstrate a reduction in CNS-infiltrating T cells, dendritic cells, and macrophages in mice lacking miR-155 expression in all cell types. I further determined, using conditional knockout mice, that although miR-155 is expressed highly throughout the immune system, not all cell types require miR-155 expression to drive EAE disease severity. Deletion of miR-155 in T cells lead to a drastic reduction in EAE disease, similar to the whole-body deletion, whereas deletion in dendritic cells lead to a less disease progression but to a lesser extent. Macrophages, while expressing high levels of miR-155, did not need miR-155 expression for full EAE disease severity. I further look into the possible interactions that DCs might have with resident glial cells during neuroinflammation to better understand how these cells could be contributing to disease. I also look into novel roles that miR-155 binding may have on non-canonical binding sites within the CDS, alternative splicing of the IL7R, and the roles of miR-155-containing extracellular vesicles during EAE.

Subject Added Entry-Topical Term  

Immunology.

Subject Added Entry-Topical Term  

Neurosciences.

Subject Added Entry-Topical Term  

Molecular biology.

Index Term-Uncontrolled  

Neuroinflammation

Index Term-Uncontrolled  

Immune cells infiltrating

Index Term-Uncontrolled  

miR-155

Index Term-Uncontrolled  

Autoimmune encephalomyelitis

Index Term-Uncontrolled  

Macrophages

Added Entry-Corporate Name  

The University of Utah Pathology

Host Item Entry  

Dissertations Abstracts International. 85-04B.

Host Item Entry  

Dissertation Abstract International

Electronic Location and Access  

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Control Number  

joongbu:643901