Host Transcriptional Regulation During a Mycobacterial Infection and Developing a Mechanism of Drug Targeting Through Folate Drug Conjugates

Master's Thesis


Mycobacterium tuberculosis, the causative agent of tuberculosis (TB), is responsible for nearly 2 million deaths each year. The rise in HIV co-infections and the neglect of TB control programs has led to TB’s re-emergence as a serious public health concern.

An improved understanding of host immune responses following Mycobacterium infection can provide insights into the pathogenesis of virulent mycobacteria and identify potential targets for rational anti-TB drug design. Our work indicates that infection with isogenic strains of M. tuberculosis results in differential activation of various transcription factors. Previous studies have demonstrated that expression of the folate receptor (FR) is primarily restricted to tumor cells and activated macrophages. We hypothesize that the FR may also be expressed on activated, tuberculosis-infected macrophages. Addressing the biology behind FR expression in Mycobacterium-infected mouse and human macrophages may lead to new mechanisms to treat drug-sensitive and drug-resistant tuberculosis.


Attribute NameValues
  • etd-12122012-211443

Author Jeannie A. Hoang
Advisor Jeffrey S. Schorey
Contributor Paul W. Huber, Committee Member
Contributor Mary Ann McDowell, Committee Member
Contributor Crislyn DSouza-Schorey, Committee Member
Contributor Jeffrey S. Schorey, Committee Chair
Degree Level Master's Thesis
Degree Discipline Biological Sciences
Degree Name MS
Defense Date
  • 2012-12-06

Submission Date 2012-12-12
  • United States of America

  • mycobacteria

  • tuberculosis

  • transcriptional regulation

  • folate receptor

  • drug development

  • University of Notre Dame

  • English

Record Visibility Public
Content License
  • All rights reserved

Departments and Units


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