Detrimental role of IRF1 in myeloid cells during Influenza infection

Author

Bianca L. Baum, Virginia Commonwealth UniversityFollow

DOI

https://doi.org/10.25772/3YB7-1N41

Author ORCID Identifier

https://orcid.org/0000-0002-4166-0094

Defense Date

2021

Document Type

Thesis

Degree Name

Master of Science

Department

Biochemistry

First Advisor

Tomasz Kordula

Abstract

The influenza virus is constantly evolving new ways to overcome both innate and vaccine-induced host defenses, making the innate immune response a critical therapeutic target for minimizing morbidity and mortality caused by infection. Here we examined the role that interferon regulatory factor 1 (IRF1) plays in regulating host innate immune responses in myeloid cells. We found that knocking out IRF1 from myeloid cells in mice (IRF1^DMy) led to a partial protection during IAV infection. Interestingly, recruitment of bone marrow derived myeloid cells as well as NLRP3 inflammasome expression were decreased in the lungs of IRF1^DMy mice, whereas expression of IFN-g was upregulated. However, expression of many chemokines and polarization of myeloid cells in the lung were unaffected. Moreover, the recruitment of bone marrow derived myeloid cells to the brain was decreased during the systemic infection. The polarization of myeloid cells in the brains of IRF1^DMy mice was not affected but the expression of IL-1b was increased. Though the mechanism by which IRF1 regulates the immune response is still not fully understood, IRF1 in myeloid cells exacerbates the innate immune response during the infection.

Rights

© The Author

Is Part Of

VCU University Archives

Is Part Of

VCU Theses and Dissertations

Date of Submission

4-29-2021