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Additional file 1: Table S1. JBI critical appraisal checklist applied for included studies

Fucose-mannose ligand (FML) is a soluble antigen purified from Leishmania donovani complex and used for diagnosis, prognosis, and vaccine development against visceral leishmaniasis (VL). We aimed to explore the effects of FML on the production of cytokines, chemokines and nitric oxide (NO) by macrophages in vitro. Peritoneal macrophages from BALB/c mice were treated with various concentrations of FML purified from Leishmania infantum in the absence or presence of LPS Peritoneal macrophages. After 48hr, cell culture supernatants were recovered and the levels of TNF-α, IL-10, IL-12p70 and IP-10 measured by Sandwich ELISA and NO concentration by Griess reaction. We found that FML significantly increase NO, IL-12p70 and IP-10 production in both LPS-treated and untreated macrophages and increase IL-10 levels only in LPS-treated macrophages. However, FML could not alert TNF-α levels in both LPS-treated and untreated macrophages. Further analysis revealed that FML can also increase IL-12p70/IL-10 ratio in LPS-treated macrophages. We concluded that FML can polarize macrophages to an appropriate phenotype similar to M1 phenotype against Leishmania donovani complex, although IL10 and TNF results are controversial.

There is no effective vaccine against malaria; therefore, chemotherapy is to date the only choice to fight against this infectious disease. However, there is growing evidences of drug-resistance mechanisms in malaria treatments. Therefore, the identification of new drug targets is an urgent need for the clinical management of the disease. Proteomic approaches offer the chance of determining the effects of antimalarial drugs on the proteome of Plasmodium parasites. Accordingly, we reviewed the effects of antimalarial drugs on the Plasmodium falciparum proteome pointing out the relevance of several proteins as possible drug targets in malaria treatment. In addition, some of the P. falciparum stage-specific altered proteins and parasite–host interactions might play important roles in pathogenicity, survival, invasion and metabolic pathways and thus serve as potential sources of drug targets. In this review, we have identified several proteins, including thioredoxin reductase, helicases, peptidyl-prolyl cis–trans isomerase, endoplasmic reticulum-resident calcium-binding protein, choline/ethanolamine phosphotransferase, purine nucleoside phosphorylase, apical membrane antigen 1, glutamate dehydrogenase, hypoxanthine guanine phosphoribosyl transferase, heat shock protein 70x, knob-associated histidine-rich protein and erythrocyte membrane protein 1, as promising antimalarial drugs targets. Overall, proteomic approaches are able to partially facilitate finding possible drug targets. However, the integration of other ‘omics’ and specific pharmaceutical techniques with proteomics may increase the therapeutic properties of the critical proteins identified in the P. falciparum proteome.

© The Author(s), 2021. The association of leishmaniasis and malignancies in human and animal models has been highlighted in recent years. The misdiagnosis of coexistence of leishmaniasis and cancer and the use of common drugs in the treatment of such diseases prompt us to further survey the molecular biology of Leishmania parasites and cancer cells. The information regarding common expressed proteins, as possible therapeutic targets, in Leishmania parasites and cancer cells is scarce. Therefore, the current study reviews proteins, and investigates the regulation and functions of several key proteins in Leishmania parasites and cancer cells. The up- and down-regulations of such proteins were mostly related to survival, development, pathogenicity, metabolic pathways and vital signalling in Leishmania parasites and cancer cells. The presence of common expressed proteins in Leishmania parasites and cancer cells reveals valuable information regarding the possible shared mechanisms of pathogenicity and opportunities for therapeutic targeting in leishmaniasis and cancers in the future. This study was supported by the National Institute for Medical Research Development (NIMAD), Tehran, Iran, grant number 971405.