Leishmania As an Eukaryotic Intracellular Organism and Its Interaction With Cells of the Immune System Publisher



Moslehi M ; Aghaei M ; Aghaei S ; Shahmoradi Z ; Iraji F ; Hejazi SH
Source: Iranian Journal of Dermatology Published:2025

Abstract

Background: Leishmaniasis, caused by the obligate intracellular parasite Leishmania, is transmitted through the bite of infected female sandflies and infects host mononuclear phagocytes, leading to cutaneous lesions or fatal visceral disease. Understanding the immune dynamics of leishmaniasis is essential for developing immunotherapies, vaccines, and control strategies. This review explores the immunological landscape of leishmaniasis, with a focus on host immune cell interactions with Leishmania and the parasite’s evasion mechanisms. Methods: We systematically reviewed articles published between 1998 and 2022 from PubMed, SciELO, ScienceDirect, Scopus, Google Scholar, and Web of Science, using the search terms “immunology” OR “leishmaniasis.” Studies on in vitro and in vivo models of Leishmania-immune cell interactions were included. Results: Protective immunity against leishmaniasis depends on Th1-mediated responses, which activates macrophages through nitric oxide (NO) production, oxidative bursts, and pro-inflammatory cytokines (e.g., IFN-γ, IL-12) to eliminate the parasite. In contrast, Th2 dominance, marked by IL-10 and TGF-β, exacerbates disease by suppressing these defenses. Leishmania employs sophisticated evasion strategies, including apoptotic mimicry and neutrophil-mediated “Trojan Horse” entry into macrophages, allowing it intracellularly and subvert host immunity. Conclusion: Elucidating the cellular interaction between Leishmania and the immune system—particularly its manipulation of apoptosis and cytokine balance—offers new avenues for innovative treatments, prevention strategies, and vaccine development against leishmaniasis. © 2025 Elsevier B.V., All rights reserved.