| Abstrakt: |
Ocular toxoplasmosis appears after primary infection or during the reactivation of chronic infection by the protozoa Toxoplasma gondii. The risk of ocular involvement and the heterogeneity of clinical manifestations, their complications, and the probability of recurrences are linked to polymorphisms in immune response-related genes, cytokine networks, lymphocyte subpopulation, and parasite virulence factors. Appropriate clinical management and evidence-based advisory recommendations for patients require a clear understanding of the immunopathological mechanisms of this parasitic disease. Narrative review of the scientific literature in human ocular toxoplasmosis related to parasitological and immunological characteristics, genetic polymorphisms linked to ocular involvement, and the clinical correlations of the cytokinome in aqueous humor and experiments with peripheral blood mononuclear cells. The greater severity in people infected by South American strains is partly explained by parasite protein kinases interfering with the effector immune functions of interferon-gamma, resulting in lower antiparasitic activity and more significant inflammation. Future therapies should point to the increase in IFN-γ production (for example, by stimulating CD4+ memory T cells subset). Thus, immune-based interventions could be promising in inducing an appropriate response for treating and preventing ocular damage and recurrences. Drugs targeting tissue cysts responsible for reactivations are a current priority. Ocular toxoplasmosis is a persistent eye condition affecting patients' visual health and quality of life. This disease may manifest after a primary infection or during the reactivation of a latent infection by the protozoan Toxoplasma gondii. In our opinion, based on the principle of precaution, all recent primary infections, symptomatic or asymptomatic, caused by Toxoplasma, should be treated, as routine screening of the susceptibility genetic factors remains unavailable. Clinicians often encounter inquiries about the source of the infection, the factors contributing to ocular involvement (which, in the majority of the population, approximately 90%, remains asymptomatic), the likelihood of recurrent episodes, and the potential expansion of ocular damage. Current scientific knowledge indicates that genetic determinants governing specific immune responses, particularly the ability to produce protective cytokines while restraining inflammatory responses, may contribute to understanding the development and characteristics of ocular toxoplasmosis in humans. The role of genetic polymorphisms has been substantiated by the analysis of cytokine profiles in aqueous humor and experimental investigations using human peripheral blood mononuclear cells (PBMCs). In South America, where virulent strains of Toxoplasma prevail, the disease can manifest itself more severely. Numerous parasite protein kinases function as virulence factors, impeding the effector immune functions of interferon-gamma, decreasing antiparasitic activity, and exacerbating inflammation. The interaction between infection by virulent strains and genetic host susceptibility factors intervene in the magnitude of retinochoroidal damage. In light of these insights, developing new therapies becomes imperative for managing and preventing recurrent ocular toxoplasmosis. Additionally, pursuing drugs capable of eradicating tissue cysts responsible for recurrences and reactivations is a current research priority. [ABSTRACT FROM AUTHOR] |
