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Leishmania donovani:Immune response and immune evasion with emphasis on PD-1/PDL-1 pathway and role of autophagy

Asian Pacific Journal of Tropical Medicine 2021年第5期14卷 195-208页

作者： Samar Habib Manar Azab Khaled Elmasry aya handoussa Department of Medical Parasitology Faculty of MedicineMansoura UniversityMansouraEgypt Department of Human Anatomy and Embryology Faculty of MedicineMansoura UniversityMansouraEgypt

Leishmania donovani is one of the causative agents of visceral leishmaniasis.The immune response against Leishmania depends on CD4^(+)T helper type 1 cells.The immune system is unable to combat Leishmania because the parasite can exert several immune suppressive mechanisms that facilitate escaping the immune responses.One of these mechanisms is the up-regulation of programmed death-1/programmed death ligand-1 pathway which causes T cells to undergo exhaustion.Autophagy is strongly linked to the immune response,with some research indicating that activating autophagy reduces the immune response to some intracellular pathogens,while others indicate that activating autophagy limits the growth of intracellular pathogens.Leishmania was found to subvert the host defense mechanisms for its own persistence,such as Leishmania-induced autophagy modulation.Leishmania was reported to activate autophagy in different studies,thus getting a dual benefit by evading the immune system and simultaneously utilizing the autophagy byproducts as nutrients.In this review,we introduced different immune evasion/suppressive mechanisms used by Leishmania,and different immunotherapies which were developed accordingly.We focused on the programmed death-1/programmed death ligand-1 pathway as well as autophagy with the potential interplay of both mechanisms.

关键词： Leishmania donovani PD-1/PDL-1 Autophagy Immune response Immunity

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Uncoupling tumor necrosis factor-αand interleukin-10 at tumor immune microenvironment of breast cancer through miR-17-5p/MALAT-1/H19 circuit

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BIOCELL 2022年第3期46卷 769-783页

作者： RAGHDA A.SOLIMAN RANA A.YOUNESS TAMER M.MANIE EMAD KHALLAF MOHAMED EL-SHAZLY MONA ABDELMOHSEN HEBA handoussa MOHAMED Z.GAD Pharmaceutical Biology Department Faculty of Pharmacy and BiotechnologyGerman University in CairoCairo11835Egypt School of Life and Medical Sciences University of Hertfordshire Hosted by Global Academic FoundationNew Administrative Capital11578Egypt Breast Surgery Department National Cancer InstituteCairo UniversityCairoEgypt General Surgery Department Faculty of MedicineCairo UniversityCairoEgypt Department of Phytochemistry National Research CentreGiza12622Egypt Biochemistry Department Faculty of Pharmacy and BiotechnologyGerman University in CairoCairo11835Egypt

Triple Negative Breast Cancer(TNBC)immunotherapy has recently shown promising approach.However,some TNBC patients presented with resistance.One of the reasons was attributed to the excessive release of cytokines at the tumor microenvironment(TME)such as Tumor necrosis factor alpha(TNF-α)and Interleukin-10(IL-10).Fine regulation of these cytokines’levels via non-coding RNAs(ncRNAs)might alleviate the immune quiescent nature of TME at TNBC tumors.However,the extrapolation of ncRNAs as therapeutic tools is highly challenging.Therefore,disentanglement the nature for the isolation of natural compounds that could modulate the ncRNAs and their respective targets is an applicable translational therapeutic approach.Hence,this study aimed to targeting the chief immune suppressive cytokines at the TME(TNF-αand IL-10)via ncRNAs and to examine the effects of Rosemary aerial parts extract on the expression levels of these ncRNAs in TNBC.Results revealed miR-17-5p as a dual regulator of TNF-αand IL-10.Moreover,an intricate interaction has been shown between miR-17-5p and the oncogenic lncRNAs:MALAT1 and H19.Knocking down of MALAT1 and/or H19 caused an induction in miR-17-5p and reduction in TNF-αand IL-10 expression levels.miR-17-5p was found to be down-regulated,while TNF-α,IL-10,MALAT1 and H19 were up-regulated in BC patients.Forced expression of miR-17-5p in MDA-MB-231 cells reduced TNF-α,IL-10,MALAT1 and H19 expression levels,as well as several BC hallmarks.In a translational approach,ursolic acid(UA)isolated from rosemary induced the expression of miR-17-5p,MALAT1 and decreased H19 expression levels.In conclusion,this study suggests miR-17-5p as a tumor suppressor and an immune-activator miRNA in BC through tuning up the immunological targets TNF-α,IL-10 at the TME and the oncological mediators MALAT1 and H19 lncRNAs.

关键词： Breast cancer Tumor microenvironment Cytokines TNF-α IL-10 miR-17-5p MALAT1 H19 lncRNAs miRNA Ursolic acid

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Pivotal role of long non-coding ribonucleic acid-X-inactive specific transcript in regulating immune checkpoint programmed death ligand 1 through a shared pathway between miR-194-5p and miR-155-5p in hepatocellular carcinoma

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World Journal of Hepatology 2020年第12期12卷 1211-1227页

作者： Sara M Atwa Heba handoussa Karim M Hosny Margarete Odenthal Hend M El Tayebi Pharmaceutical Biology Department German University in CairoCairo 11865Egypt Department of General Surgery Faculty of MedicineCairo UniversityCairo 11562Egypt Institute for Pathology University Hospital CologneCologne 50924Germany Molecular Pharmacology Research Group Department of Pharmacology and ToxicologyFaculty of Pharmacy and BiotechnologyGerman University in CairoCairo 11835Egypt

BACKGROUND Anti-programmed death therapy has thrust immunotherapy into the spotlight.However,such therapy has a modest response in hepatocellular carcinoma(HCC).Epigenetic immunomodulation is a suggestive combinatorial therapy with immune checkpoint blockade.Non-coding ribonucleic acid(ncRNA)driven regulation is a major mechanism of epigenetic modulation.Given the wide range of ncRNAs that co-opt in programmed cell-death protein 1(PD-1)/programmed death ligand 1(PD-L1)regulation,and based on the literature,we hypothesized that miR-155-5p,miR-194-5p and long non-coding RNAs(lncRNAs)X-inactive specific transcript(XIST)and MALAT-1 are involved in a regulatory upstream pathway for PD-1/PD-L1.Recently,nutraceutical therapeutics in cancers have received increasing attention.Thus,it is interesting to study the impact of oleuropein on the respective study key players.AIM To explore potential upstream regulatory ncRNAs for the immune checkpoint PD-1/PD-L1.METHODS Bioinformatics tools including *** and lnCeDB software were adopted to detect targeting of miR-155-5p,miR-194-5p and lncRNAs XIST and MALAT-1 to PD-L1 mRNA,respectively.In addition,Diana tool was used to predict targeting of both aforementioned miRNAs to lncRNAs XIST and MALAT-1.HCC and normal tissue samples were collected for scanning of PD-L1,XIST and MALAT-1 expression.To study the interaction among miR-155-5p,miR-194-5p,lncRNAs XIST and MALAT-1,as well as PD-L1 mRNA,a series of transfections of the Huh-7 cell line was carried out.RESULTS Bioinformatics software predicted that miR-155-5p and miR-194-5p can target PDL1,MALAT-1 and XIST.MALAT-1 and XIST were predicted to target PD-L1 mRNA.PD-L1 and XIST were significantly upregulated in 23 HCC biopsies compared to healthy controls;however,MALAT-1 was barely detected.MiR-194 induced expression elevated the expression of PD-L1,XIST and MALAT-1.However,overexpression of miR-155-5p induced the upregulation of PD-L1 and XIST,while it had a negative impact on MALAT-1 expression.Knockdown of XIST did have an impact on

关键词： Hepatocellular carcinoma X-inactive specific transcript MiR-155-5p MiR-194-5p Programmed cell-death protein 1/Programmed death ligand 1 Immune checkpoint

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