Galectin-1 Reduces the Severity of Herpes Simplex Virus-Induced Ocular Immunopathological Lesions

The Journal of Immunology, 04/23/2012

The authors findings are the first to show that galectin–1 (gal–1) treatment represents a useful approach to control lesion severity in a virally induced immunopathological disease.

Author Commentary

Controlling chronic immunopathological lesions in the eye such as those caused by ocular herpes simplex virus-1 (HSV) infection remains a major therapeutic challenge. HSV induced stromal keratitis (SK) lesions are thought to be primarily orchestrated by CD4+ T cells of the Th1 subtype with some involvement of Th17 CD4+ T cells. One therapeutic strategy would be to suppress the function of effector CD4+ T cell subsets and the events they orchestrate, as we demonstrate can be achieved by galectin-1 (gal-1) treatment. Our data showed that treatment with recombinant gal-1 significantly diminished SK lesion severity and the extent of corneal neovacularization. The beneficial effect of gal-1 was the consequence of multiple mechanisms. These included apoptotic effects on pro-inflammatory T cells, reduced recruitment of tissue-damaging neutrophils, inhibitory effects on inflammatory cytokine and chemokine production, an increased production of the anti-inflammatory IL-10, as well as an inhibitory effect on the corneal neovascularization needed for inflammatory cells to access the corneal stroma. Our results indicate that gal-1 treatment may represent a useful approach to control HSV-induced ocular lesions, the most common infectious cause of blindness in the western world.

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