Biomedical Sciences ETDs
Publication Date
Fall 12-15-2026
Abstract
Chronic hypoxia (CH), caused by sleep apnea, chronic obstructive pulmonary disease, or high-altitude exposure, leads to pulmonary hypertension (PH). The pathogenesis of CH-induced PH has a number of hallmarks, including phenotypic changes in the pulmonary smooth muscle cells, arterial wall thickening, enhanced vasoreactivity, and inflammation around the pulmonary arteries. Utilizing a T regulatory (Treg) cell lineage tracking mouse model, this dissertation sought to further establish the importance of Treg and T helper 17 (TH17) cell balance in CH-induced PH. We demonstrated that Treg number and suppressive capacity decrease, TH17 cells increase, and Treg-to-TH17 cell transition occurs following exposure to hypoxia. We also show evidence that inducing tolerance to collagen type V (col V), a known self-antigen, attenuates indices of CH-induced PH. Altogether, this work further elucidates the mechanisms of the inflammatory response and possible therapeutic targets for preventing and treating CH-induced PH.
Keywords
Immune cell balance, Pulmonary hypertension, Treg, exTreg, Immune Tolerance
Document Type
Dissertation
Language
English
Degree Name
Biomedical Sciences
Level of Degree
Doctoral
Department Name
Biomedical Sciences Graduate Program
First Committee Member (Chair)
Jay Naik
Second Committee Member
Laura Gonzalez Bosc
Third Committee Member
Tom Resta
Fourth Committee Member
Meilian Liu
Recommended Citation
Lantz, Benjamin. "IMMUNE CELL BALANCE IN CHRONIC HYPOXIA INDUCED PULMONARY HYPERTENSION." (2026). https://digitalrepository.unm.edu/biom_etds/269
Included in
Cell Biology Commons, Cellular and Molecular Physiology Commons, Medicine and Health Sciences Commons
