Keywords

autoimmunity; immunology; melanoma; dermatology; regeneration; UV damage; Photo-damage; innate immunity

Abstract

Ultraviolet radiation is an environmental stressor known to suppress immune function in the skin, but its effect on the immunoregulatory M2 phenotype macrophages is poorly studied. This study aims to investigate the impact of UV exposure on key markers of the M2 macrophage, which are critical for tissue repair and immunosuppression. THP-1 monocytes were differentiated and polarized into the M2 phenotype using Phorbol-12 myristate (PMA) and Cytokines IL-4 and IL-10. Once differentiation was confirmed, the macrophages were exposed to varying durations of UV radiation. Real Time Quantitative PCR was used to analyze expression changes in phagocytic receptors (CD206, CD163, Arg-1), prototypic marker (CHI3L1/YKL-40), and immunosuppressive mediator (PD-L1). Further, western blot was used to check for post translational upregulation or down regulation of Arginase-1 and TGF-β. Results show a significant, time dependent downregulation of M2 marker expression following UV exposure. The down regulation was particularly pronounced for the CD206 phagocytic receptor and the Arginase-1 after exposure exceeding 90 seconds. This suggests that these pathways involved in nitric oxide metabolism are most vulnerable to UV disruption. This indicates that UV radiation broadly disrupts the M2 phenotype, compromising both its phagocytic and immunomodulatory function. This experiment reveals a new mechanism of UV induced immunosuppression and identifies the M2 macrophage as a key target, providing insight into UV related pathogenesis of chronic inflammation and impaired wound healing in photodamaged skin.

Thesis Completion Year

2025

Thesis Completion Semester

Fall

Thesis Chair

Borgon, Robert

College

College of Medicine

Thesis Discipline

Biomedical Science

Language

English

Access Status

Open Access

Length of Campus Access

None

Campus Location

Orlando (Main) Campus

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Rights Statement

In Copyright