Abstract
The intracellular protozoan parasites of the genus Leishmania are the causative agents of leishmaniasis, a vector-borne disease of major public health concern, estimated to affect 12 million people worldwide. The clinical manifestations of leishmaniasis are highly variable and can range from self-healing localized cutaneous lesions to life-threatening disseminated visceral disease. Once introduced into the skin by infected sandflies, Leishmania parasites interact with a variety of immune cells, such as neutrophils, monocytes, dendritic cells (DCs), and macrophages. The resolution of infection requires a finely tuned interplay between innate and adaptive immune cells, culminating with the activation of microbicidal functions and parasite clearance within host cells. However, several factors derived from the host, insect vector, and Leishmania spp., including the presence of a double-stranded RNA virus (LRV), can modulate the host immunity and influence the disease outcome. In this review, we discuss the immune mechanisms underlying the main forms of leishmaniasis, some of the factors involved with the establishment of infection and disease severity, and potential approaches for vaccine and drug development focused on host immunity.
Highlights
Leishmania is the genus of more than 20 digenetic protozoan parasites from the Trypanosomatidae family that causes the vector-borne diseases collectively known as leishmaniasis, a serious public health problem with estimated 0.7–1 million new cases per year [1,2,3]
More than 90% of mucocutaneous leishmaniasis (MCL) cases have been reported in three South American countries (Brazil, Peru, and Bolivia) and, other Leishmania spp. are associated with this manifestation, such as L. major, L. panamensis, L. tropica, and L. infantum, MCL has been commonly observed in L. braziliensis infections [2,5]
Once inoculated into the host dermis by an infected sandfly, infective metacyclic promastigotes of Leishmania are engulfed by a variety of immune cells, such as resident dermal dendritic cells, macrophages and infiltrating neutrophils that act as the first line of defense [20,21,22,23,24]
Summary
Leishmania is the genus of more than 20 digenetic protozoan parasites from the Trypanosomatidae family that causes the vector-borne diseases collectively known as leishmaniasis, a serious public health problem with estimated 0.7–1 million new cases per year [1,2,3]. The type and severity of the clinical manifestations are mostly determined by the infecting Leishmania spp. Other factors, such as vector biology and host immune status, greatly influence the disease outcome [5]. Once in a mammalian host, promastigotes rapidly differentiate into non-motile round-shaped amastigotes within mononuclear phagocytes, where they proliferate and establish infection in phagosomes [6,7]. The clearance of these intracellular parasites and, the infection resolution involves the coordinated participation of both innate and adaptive immunity, a process that demands precise regulation. We will review the immune mechanisms driving the diverse clinical forms of leishmaniasis, focusing on the factors that contribute to disease severity and potential approaches to circumvent these limitations
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