Abstract
Cutaneous leishmaniasis exhibits a wide spectrum of clinical presentations from self-resolving infections to severe chronic disease. Anti-parasitic drugs are often ineffective in the most severe forms of the disease, and in some cases the magnitude of the disease can result from an uncontrolled inflammatory response rather than unrestrained parasite replication. In these patients, host-directed therapies offer a novel approach to improve clinical outcome. Importantly, there are many anti-inflammatory drugs with known safety and efficacy profiles that are currently used for other inflammatory diseases and are readily available to be used for leishmaniasis. However, since leishmaniasis consists of a wide range of clinical entities, mediated by a diverse group of leishmanial species, host-directed therapies will need to be tailored for specific types of leishmaniasis. There is now substantial evidence that host-directed therapies are likely to be beneficial beyond autoimmune diseases and cancer and thus should be an important component in the armamentarium to modulate the severity of cutaneous leishmaniasis.
Highlights
Cutaneous leishmaniasis is caused by several different species of protozoa transmitted by sand flies, and has a variety of clinical forms, ranging from self-healing lesions to chronic disfiguring mucosal disease [1, 2]
In some cases, the lesions fail to resolve, or the parasites spread to many cutaneous sites without any evidence of control, a form of leishmaniasis known as diffuse cutaneous leishmaniasis (DCL) [8,9,10]
lymphocytic choriomeningitis virus (LCMV) specific NKG2D expressing CD8 T cells were recruited to the cutaneous lesions non- and mediated killing of targets expressing NKG2D ligands that were upregulated on cells in the lesions due to inflammation
Summary
Cutaneous leishmaniasis is caused by several different species of protozoa transmitted by sand flies, and has a variety of clinical forms, ranging from self-healing lesions to chronic disfiguring mucosal disease [1, 2]. Host-directed therapies for infectious diseases are designed to either amplify protective immune responses, divert non-protective immune responses towards protective responses, or block pathologic immune responses [5]. Our in-depth understanding of both protective and pathologic immune responses and identification of agents that can be used clinically to influence immune responses has revolutionized treatment of a wide range of diseases. While many of these new treatments are for non-communicable diseases, repurposing such treatments for infectious diseases, such as cutaneous leishmaniasis is advantageous, as their safety and efficacy profiles have often already been established
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