UVB radiation impairs CD4+ and IFNγ+ cell responses, promoting IL-10+ cells and exacerbating lesions caused by Leishmania mexicana using a mouse model 30 days post-infection.

In mice, susceptibility or resistance to Leishmania spp. infection is associated with distinct CD4+ T-helper cell responses. A predominant Th2 response, characterized by chronic disease, contrasts with a Th1 response, which promotes healing and parasite clearance. Ultraviolet B (UVB) radiation induces local and systemic immunosuppression by impairing antigen-presenting cell function, stimulating IL-10 production, and skewing the Th1/Th2 balance towards a Th2 phenotype dominated by IL-4 and IL-10. This study investigated disease progression and early local immune responses in UVB-immunosuppressed C57BL/6 mice infected with Leishmania mexicana. Mice were exposed to immunosuppressive doses of UVB radiation and subsequently infected with L. mexicana promastigotes. Lesion size, parasite load, histopathology, and the presence of IL-10+, IFN-γ+, mast cells, macrophages (MOMA2+), CD4+, and CD8+ T cells at the lesion site were evaluated. UVB-exposed, L. mexicana-infected mice exhibited altered tissue architecture, increased numbers of both intact and degranulated mast cells, and elevated IL-10+ and MOMA2+ cell infiltration in skin lesions, compared to wild-type, L. mexicana-infected controls. Conversely, CD4+, CD8+, and IFN-γ+ cells were decreased in the UVB-exposed group. These findings suggest that exposure to UVB radiation acts as a risk factor for cutaneous leishmaniasis (LCL), as these findings indicate it can exacerbate lesions and increase parasite load through the induction of an unfavorable immune microenvironment.