Immunology and Genetic of Leishmania infantum: The Role of Endonuclease G in the Apoptosis

Leishmania infantum is the causative agent of infantile visceral leishmaniasis (VL) in the Mediterranean region. Despite developing protective responses, the disease progresses due to many of factors. Tese include the action of suppressive cytokines, exhaustion of specifc T cells, loss of lymphoid tissue, and defective humoral response. Genetic changes that occur inside the genome of alienated or parasite cells, along with immune responses, play an important role in controlling or progressing the disease. Proapoptotic proteins such as Smac/DIABLO, EndoG, AIF (apoptosis?inducing factor), and cytochrome C are e?ective in apoptosis. EndoG is a mitochondrion?specifc nuclease that translocates to the nucleus during apoptosis. Once released from mitochondria, endoG cleaves chromatin DNA into nucleosomal fragments independently of caspases. Terefore, endoG represents a caspase?independent apoptotic pathway initiated from the mitochondria. A comprehensive understanding of the immune and genetic events that occur during VL is very important for designing immunotherapy strategies and developing e?ective vaccines for disease prevention. In this review which explained the immunological responses and also the important factors that can contribute to parasite apoptosis and are used in subsequent studies as a target for the reparation of drugs or recombinant vaccines against parasites are brie?y reviewed.